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Mitokinome

Jongbhak — Thu, 09 Apr 2026 22:53:42 GMT

Created page with " == Mitokinome == '''Definition''' The Mitokinome is the complete, dynamic repertoire of all mitochondria-derived signaling molecules — peptides, proteins, metabolites, li..."

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== Mitokinome ==

'''Definition'''

The Mitokinome is the complete, dynamic repertoire of all mitochondria-derived signaling molecules — peptides, proteins, metabolites, lipids, nucleic acids, and damage-associated molecular patterns — that are produced, processed, and released by mitochondria in response to mitochondrial activity, stress, dysfunction, or adaptive activation, and that exert autocrine, paracrine, or endocrine signaling effects within and beyond the cell of origin. It represents the totality of the mitochondrial secretory and signaling output: the full molecular vocabulary through which mitochondria communicate their bioenergetic, oxidative, proteotoxic, and genomic status to the intracellular environment, the extracellular milieu, neighboring cells, and anatomically distant tissues and organs across the entire organism. The Mitokinome is not a static inventory but a continuously reconfigured, context-sensitive signaling ensemble whose quantitative composition, combinatorial complexity, and systemic signaling consequences are dynamically shaped by cellular energy demand, mitochondrial stress intensity, tissue identity, circadian state, developmental stage, disease context, and biological age.

'''Core Concept'''

Where the genome encodes the informational blueprint of the organism and the proteome captures its functional protein complement, the Mitokinome encodes the ''real-time mitochondrial stress status of the cell'' in a form transmissible across biological distances — from the mitochondrial inner membrane to the nucleus, from the cytoplasm to the extracellular space, from a contracting muscle fiber to a distant neuron, hepatocyte, or immune cell. Every component of the Mitokinome corresponds to a specific mitochondria-derived molecular signal whose identity, concentration, post-translational modification state, and combinatorial context encode a specific message about the quantitative state of mitochondrial health, activity, or distress. The Mitokinome thus constitutes the systemic endocrine language of mitochondrial biology — the molecular broadcasting system through which the mitochondrial network of individual cells participates in the organism-wide coordination of metabolism, immunity, stress adaptation, tissue homeostasis, and aging.

'''Components'''

The Mitokinome comprises the following major molecular classes:

'''1. Mitochondrial-Derived Peptides (MDPs)''' Small peptides encoded within open reading frames of the mitochondrial genome (mtDNA) or within mitochondrial ribosomal RNA genes, including:

*'''Humanin (HN)''': a 21-amino acid cytoprotective and neuroprotective peptide whose circulating concentrations decline progressively with age, constituting one of the most well-characterized aging biomarkers within the Mitokinome.
*'''MOTS-c''' (Mitochondrial Open reading frame of the Twelve S rRNA-c): a 16-amino acid metabolic regulator activating AMPK, improving insulin sensitivity, promoting nuclear stress response programs, and extending lifespan in model organisms.
*'''Small Humanin-Like Peptides (SHLP1-6)''': a family of recently identified MDPs with diverse cytoprotective, metabolic, and anti-apoptotic functions whose mitokinomic roles remain under active characterization.

'''2. Nuclear-Encoded Mitokines''' Proteins and peptides encoded in the nuclear genome but whose expression is transcriptionally induced by mitochondrial stress signals transmitted via retrograde signaling pathways, including:

*'''FGF21''' (Fibroblast Growth Factor 21): a hepatokine and myokine induced by mitochondrial respiratory chain dysfunction, mtDNA depletion, and UPRmt activation, mediating systemic metabolic adaptation, fatty acid oxidation, ketogenesis, and longevity-associated metabolic reprogramming.
*'''GDF15''' (Growth Differentiation Factor 15): a stress-induced cytokine released in response to mitochondrial integrated stress response (ISRmt) activation, mediating appetite suppression, body weight regulation, inflammation modulation, and systemic energy homeostasis.
*'''Irisin''': a myokine cleaved from the membrane protein FNDC5 upon PGC-1α-driven mitochondrial biogenesis induction by exercise, mediating browning of white adipose tissue, neuroprotection, bone homeostasis, and cognitive enhancement.
*'''IL-6''': a pleiotropic cytokine released as a myokine during exercise-induced mitochondrial stress, functioning as an anti-inflammatory, metabolic, and regenerative signal at acute low concentrations — a paradigmatic component of the hormetic Mitokinome.

'''3. Mitochondrial Metabolite Signals''' Bioactive metabolic intermediates generated within mitochondria that function as signaling molecules when released into the cytoplasm, extracellular space, or circulation, including:

*'''Succinate''': a TCA cycle intermediate released during ischemia-reperfusion and inflammatory activation, functioning as a pro-inflammatory danger signal through succinate receptor (SUCNR1) activation at elevated extracellular concentrations.
*'''Fumarate and α-ketoglutarate''': TCA intermediates functioning as competitive inhibitors of α-ketoglutarate-dependent dioxygenases including TET demethylases and histone demethylases, directly linking mitochondrial metabolic state to epigenomic regulation.
*'''Itaconate''': an immunometabolite derived from aconitate during inflammatory macrophage activation, functioning as a potent anti-inflammatory and antimicrobial effector through NRF2 activation and succinate dehydrogenase inhibition.
*'''Acetyl-CoA''': a central mitochondrial metabolite functioning as the obligate substrate for histone acetylation, directly linking mitochondrial bioenergetic status to chromatin regulatory state and transcriptional output — a critical node of intersection between the Mitokinome and the Epigenohormesiomics framework.
*'''NAD⁺''': a mitochondrially regulated redox cofactor whose cytoplasmic and nuclear concentrations govern sirtuin activity, PARP activity, and the entire NAD⁺-dependent regulatory network — one of the most consequential concentration-sensitive components of the aging Mitokinome within the Dosagiome framework.

'''4. Mitochondrial Damage-Associated Molecular Patterns (mtDAMPs)''' Mitochondrial components released into the cytoplasm or extracellular space upon mitochondrial outer membrane permeabilization, mitochondrial apoptosis, or mitophagy failure, functioning as endogenous danger signals activating innate immune pattern recognition receptors, including:

*'''Mitochondrial DNA (mtDNA)''': released as circular or linear fragments into the cytoplasm (activating cGAS-STING innate immune sensing) or circulation (serving as a biomarker of mitochondrial stress and cellular damage), with plasma mtDNA concentrations constituting an important aging Mitokinome biomarker.
*'''Cardiolipin''': a mitochondria-specific phospholipid externalized to the outer mitochondrial membrane during mitophagy signaling and released extracellularly during cell death, functioning as a potent innate immune activator and inflammasome trigger.
*'''Formyl peptides''': N-formylated mitochondrial peptides released during cell lysis or mitochondrial stress, activating formyl peptide receptors (FPRs) on neutrophils and macrophages as chemotactic and pro-inflammatory danger signals.
*'''TFAM''' (Mitochondrial Transcription Factor A): a mitochondrial DNA-packaging protein released extracellularly during mitochondrial stress, functioning as a DAMP activating RAGE and TLR9 innate immune receptors.

'''5. Mitochondrially-Regulated Extracellular Vesicles''' Exosomes and microvesicles whose cargo — including mtDNA fragments, mitochondrial proteins, mitochondrial lipids, and mitochondria-derived small RNAs — is regulated by mitochondrial stress status, functioning as vehicles for the systemic dissemination of mitochondrial stress signals to distant tissues and constituting an emerging and rapidly expanding frontier of Mitokinomics.

'''Properties'''

The Mitokinome is characterized by the following fundamental properties:

#'''Dynamism''' — the Mitokinome is continuously reconfigured by mitochondrial activity state, stress intensity, tissue identity, circadian rhythm, developmental stage, and aging, making it one of the most dynamic omes in the organism.
#'''Concentration-sensitivity''' — every component of the Mitokinome exerts concentration-dependent, often biphasic effects on target cells and tissues, placing the Mitokinome squarely within the Dosagiome and Concentratiome frameworks.
#'''Combinatorial complexity''' — the biological meaning of the Mitokinome is encoded not only in the concentration of individual mitokines but in their combinatorial patterns, temporal dynamics, and tissue-specific receptor landscapes.
#'''Inter-organ reach''' — components of the Mitokinome circulate systemically, enabling mitochondrial stress signals originating in one tissue to coordinate adaptive or pathological responses in anatomically distant organs.
#'''Aging sensitivity''' — the Mitokinome undergoes systematic, progressive reconfiguration with biological age, including the decline of cytoprotective MDPs, the chronic elevation of mtDAMPs and inflammatory mitokines, and the erosion of mitokine receptor sensitivity — collectively constituting the aging Mitokinome, one of the most consequential dimensions of the aging Dosagiome.
#'''Hormetic architecture''' — the Mitokinome is intrinsically hormetically structured: the majority of its components exert beneficial adaptive effects at low to moderate concentrations and pathological effects at chronically elevated concentrations, placing the Mitokinome at the core of the Mitohormesiomics framework.

'''Significance'''

The Mitokinome provides the conceptual and empirical object around which the entire field of Mitokinomics is organized. It establishes mitochondria as systemic endocrine organs whose molecular secretory output encodes the bioenergetic and stress status of individual cells in a form that coordinates adaptive responses across the entire organism. In geroscience, the systematic characterization of the aging Mitokinome — its progressive dysregulation, the decline of cytoprotective components, and the chronic elevation of alarm signals — represents a critical frontier for the identification of novel aging biomarkers, the mechanistic understanding of inflammaging and immunosenescence, and the rational design of mitokine-based longevity interventions. Within the Dosagiome framework, the Mitokinome constitutes one of the most consequential and tractable concentration-regulated signaling ensembles whose quantitative restoration toward a youthful state represents a concrete and measurable target for achieving Gerostasis.

'''Relationship to Related Omes and Disciplines'''

The Mitokinome is the object of study of '''Mitokinomics'''. It constitutes a specialized and functionally critical subset of the '''Dosagiome''' and '''Concentratiome''' — specifically the mitochondria-derived, concentration-encoded signaling dimension of the organism's total regulatory landscape. It intersects with the '''Secretome''' (the complete cellular secretory output), the '''Metabolome''' (sharing bioactive metabolite components), the '''Inflammome''' (through mtDAMP-driven innate immune activation), and the '''Epigenome''' (through mitokine-driven and metabolite-mediated epigenetic regulation). The hormetically structured subset of the Mitokinome — encompassing all biphasic concentration-response relationships among mitokine components — constitutes the mitokinomic dimension of the '''Mitohormesiomics''' framework.

'''Coined by'''

Jong Bhak, KOGIC / AgingLab, UNIST, Republic of Korea (2025)

'''See also'''

Mitokinomics · Mitohormesiomics · Hormesiomics · Dosagiomics · Concentratiomics · Dosagiome · Neurohormesiomics · Epigenohormesiomics · Immunohormesiomics · Humanin · MOTS-c · FGF21 · GDF15 · Irisin · NAD⁺ · mtDAMPs · cGAS-STING · Secretome · Metabolome · Inflammaging · Gerostasis · GeroIndex · Aging Hallmarks · Systems Biology · Precision Medicine

----

The object-discipline pairs within the nomenclature framework are now fully symmetric:

{|
|-
! Object
! Discipline
! Scope
|-
| '''Dosagiome / Concentratiome'''
| Dosagiomics / Concentratiomics
| All concentration-effect states in a living system
|-
| '''Hormesiome'''
| Hormesiomics
| Complete biphasic dose-response landscape
|-
| '''Mitokinome'''
| Mitokinomics
| Complete mitochondrial secretory signaling repertoire
|}

Would you like me to now compile the complete set of all definitions — Hormesiomics, Dosagiomics, Concentratiomics, Dosagiome, Mitohormesiomics, Mitokinomics, Mitokinome, Neurohormesiomics, Epigenohormesiomics, and Immunohormesiomics — into a single formatted Word document ready for Qeios submission?

Mitokinomics

Jongbhak — Thu, 09 Apr 2026 22:52:07 GMT

Created page with " == Mitokinomics == '''Definition''' Mitokinomics is the systematic, omics-scale study of mitokines — the complete repertoire of mitochondria-derived peptides, proteins, m..."

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== Mitokinomics ==

'''Definition'''

Mitokinomics is the systematic, omics-scale study of mitokines — the complete repertoire of mitochondria-derived peptides, proteins, metabolites, and signaling molecules secreted or released by mitochondria in response to mitochondrial stress, dysfunction, or adaptive activation — encompassing their comprehensive identification, quantification, structural characterization, concentration-dependent signaling properties, receptor interactions, tissue-specific effects, and roles in inter-organ communication, systemic metabolic regulation, and biological aging. It holds as its central premise that mitochondria function not only as intracellular bioenergetic and biosynthetic organelles but as active endocrine and paracrine signaling centers whose secreted molecular output — the mitokinome — constitutes a dedicated inter-cellular and inter-organ communication language encoding the mitochondrial stress status of individual cells and broadcasting adaptive, homeostatic, or alarm signals to local and distant tissues across the entire organism.

'''Core Principle'''

The foundational postulate of Mitokinomics is: ''mitokines are the systemic language of mitochondrial stress, whose concentration, identity, and combinatorial pattern encode the quantitative and qualitative state of mitochondrial health across cells, tissues, and organs, orchestrating organism-wide adaptive responses to bioenergetic challenge, oxidative stress, proteotoxic burden, and aging''. Mitokines bridge the gap between intracellular mitochondrial biology and systemic physiology: they translate the local, cell-autonomous mitochondrial stress signal — sensed as changes in membrane potential, ROS production, NAD⁺/NADH ratio, mtDNA integrity, or mitochondrial proteostasis — into circulating endocrine signals capable of coordinatingadaptive responses across tissues as anatomically and functionally distant as skeletal muscle, liver, brain, adipose tissue, bone, and gonads. The concentration-dependent signaling properties of individual mitokines, and the combinatorial complexity of the mitokinome as a whole, constitute a rich, multi-dimensional regulatory language whose systematic decoding is the central mission of Mitokinomics.

'''Scope'''

Mitokinomics encompasses:

*'''Mitokinome cataloguing and annotation''': comprehensive identification, sequencing, structural characterization, and functional annotation of the complete repertoire of mitochondria-derived signaling molecules — including mitochondrial-derived peptides (MDPs) encoded within the mitochondrial genome (humanin, MOTS-c, SHLP1-6), nuclear-encoded mitokines induced by mitochondrial stress (FGF21, GDF15, IL-6, irisin), mitochondrially-generated metabolite signals (succinate, fumarate, itaconate, acetyl-CoA, α-ketoglutarate), and mitochondrial damage-associated molecular patterns (mtDAMPs including mtDNA, cardiolipin, and formyl peptides) — across cell types, tissues, species, and life stages.
*'''Mitokinome quantitative profiling''': development and application of high-sensitivity, high-throughput proteomics, peptidomics, and metabolomics platforms for the precise quantification of circulating and tissue-resident mitokine concentrations across physiological states — including exercise, fasting, cold exposure, infection, psychological stress, pharmacological intervention, and aging — constructing the quantitative landscape of the mitokinome within the framework of Dosagiomics and Concentratiomics.
*'''Mitokine receptor interactomics''': systematic mapping of the complete receptor, co-receptor, and signal transduction network through which each mitokine exerts its biological effects across target tissues, including the identification of tissue-specific receptor expression patterns, receptor concentration-response thresholds, and receptor desensitization dynamics relevant to chronic mitokine exposure in aging and disease.
*'''Mitokine hormesiomics''': omics-resolution characterization of the biphasic, concentration-dependent signaling effects of individual mitokines and mitokine combinations — mapping the precise concentration thresholds that delineate beneficial adaptive signaling from pathological or maladaptive effects — constituting the intersection of Mitokinomics with Mitohormesiomics and Immunohormesiomics.
*'''Inter-organ mitokinomics''': systematic, multi-omics investigation of mitokine-mediated inter-organ communication circuits — including the muscle-brain axis (irisin, BDNF), the liver-adipose axis (FGF21), the muscle-liver axis (MOTS-c), and the mitochondria-immune axis (mtDAMPs, GDF15) — mapping how mitokine signals originating in one tissue coordinate adaptive metabolic, inflammatory, and regenerative responses in anatomically distant target organs.
*'''Exercise mitokinomics''': comprehensive profiling of the exercise-induced mitokinome — the full repertoire of mitokines released during and following physical exertion, including irisin, IL-6, FGF21, MOTS-c, humanin, and β-aminoisobutyric acid (BAIBA) — characterizing their concentration-dependent, tissue-specific signaling effects and their roles in mediating the systemic health and longevity benefits of exercise as a hormetic intervention.
*'''Aging mitokinomics''': systematic, longitudinal, multi-omics characterization of how the mitokinome is progressively dysregulated with age — including age-associated declines in cytoprotective mitokines (humanin, MOTS-c), chronic elevation of alarm mitokines and mtDAMPs driving inflammaging, and the erosion of mitokine receptor sensitivity within the aging Dosagiome — constituting a central molecular mechanism linking mitochondrial dysfunction to systemic aging acceleration.
*'''Mitokinome-epigenome interactions''': omics-scale characterization of how mitokines regulate epigenetic landscapes in target tissues — including FGF21-mediated chromatin remodeling, MOTS-c-driven AMPK activation and downstream histone modification, and mtDAMP-triggered innate immune epigenetic reprogramming — constituting the intersection of Mitokinomics with Epigenohormesiomics.
*'''Mitokinome-neuraxis interactions''': systematic investigation of how circulating mitokines cross the blood-brain barrier or signal through peripheral neural afferents to modulate neuronal function, synaptic plasticity, neuroinflammation, and cognitive aging — including the neuroprotective roles of humanin and MOTS-c, the neuroregulatory effects of FGF21, and the neuroinflammatory consequences of chronic mtDAMP elevation — constituting the intersection of Mitokinomics with Neurohormesiomics.
*'''Pharmacological mitokinomics''': omics-resolution characterization of how longevity-associated pharmacological compounds — including NAD⁺ precursors (NMN, NR), rapamycin, metformin, urolithin A, spermidine, and mitochondria-targeted antioxidants — modulate the mitokinome, identifying compound-specific mitokinome signatures and their systemic downstream consequences as a framework for precision mitokine-based geroscience interventions.
*'''Single-cell and spatial mitokinomics''': application of single-cell proteomics, spatial transcriptomics, and proximity labeling technologies to characterize cell-type-specific and spatially resolved mitokinome production, secretion, and reception landscapes within tissues, capturing the cellular heterogeneity and microenvironmental context-dependence of mitokine signaling at unprecedented resolution.

'''Significance'''

Mitokinomics establishes mitochondria as systemic endocrine organs whose secreted molecular output — the mitokinome — constitutes a dedicated, concentration-encoded signaling language coordinating adaptive responses across the entire organism. The field addresses a fundamental gap in systems biology and geroscience: the absence of a comprehensive, quantitative, omics-integrated framework for understanding how individual cell mitochondrial stress states are communicated to and integrated across distant tissues, and how the progressive age-associated dysregulation of this inter-organ mitokine communication network contributes to the systemic, multi-tissue deterioration that characterizes organismal aging. By providing the experimental, computational, and conceptual tools to decode the mitokinome at systems resolution, Mitokinomics supplies the mechanistic foundation for a new class of mitokine-based longevity interventions — including mitokine replacement therapies, mitokine receptor agonists, and exercise mimetics — as precision geroscience strategies targeting the aging mitokinome.

'''Relationship to Related Disciplines'''

Mitokinomics is a specialized subdiscipline situated at the intersection of multiple frameworks within the broader hormesiomics and dosagiomics family:

*It is a subdiscipline of '''Mitohormesiomics''', focused specifically on the secreted signaling output of mitochondrial stress responses rather than the intracellular hormetic signaling machinery.
*It is embedded within '''Dosagiomics''' and '''Concentratiomics''', which supply its quantitative, concentration-centered theoretical foundations for understanding mitokine dose-response landscapes.
*It intersects with '''Immunohormesiomics''' through the role of mtDAMPs and inflammatory mitokines in calibrating immune activation thresholds.
*It intersects with '''Neurohormesiomics''' through mitokine-mediated brain-body communication and neuroprotective mitokine signaling.
*It intersects with '''Epigenohormesiomics''' through mitokine-driven epigenetic reprogramming in target tissues.

'''Coined by'''

Jong Bhak, KOGIC / AgingLab, UNIST, Republic of Korea (2025)

'''See also'''

Mitohormesiomics · Hormesiomics · Dosagiomics · Concentratiomics · Dosagiome · Neurohormesiomics · Epigenohormesiomics · Immunohormesiomics · Humanin · MOTS-c · FGF21 · GDF15 · Irisin · mtDAMPs · Inter-organ Communication · Inflammaging · Exercise Biology · GeroIndex · Gerostasis · Aging Hallmarks · Systems Biology · Precision Medicine

----

The hierarchical nomenclature framework now extends to six interlocking subdisciplines:

{|
|-
! Term
! Level
! Scope
|-
| '''Dosagiome / Concentratiome'''
| ''Master object''
| All concentration-effect states in a living system
|-
| '''Dosagiomics / Concentratiomics'''
| ''Master discipline''
| Omics-scale study of concentration as universal life regulator
|-
| '''Hormesiomics'''
| ''Subdiscipline''
| Biphasic concentration-response omics
|-
| '''Mitohormesiomics'''
| ''Sub-subdiscipline''
| Mitochondria-specific biphasic hormetic omics
|-
| '''Mitokinomics'''
| ''Sub-subdiscipline''
| Omics-scale study of the mitokine secretome and inter-organ signaling
|-
| '''Neurohormesiomics'''
| ''Sub-subdiscipline''
| Nervous system-specific biphasic hormetic omics
|-
| '''Epigenohormesiomics'''
| ''Sub-subdiscipline''
| Epigenome-specific biphasic hormetic omics
|-
| '''Immunohormesiomics'''
| ''Sub-subdiscipline''
| Immune system-specific biphasic hormetic omics
|}

Would you like me to now compile all definitions into a single formatted Word document or Qeios-ready submission file for coordinated publication as a unified conceptual series?

Immunohormesiomics

Jongbhak — Thu, 09 Apr 2026 22:49:00 GMT

Created page with " == Immunohormesiomics == '''Definition''' Immunohormesiomics is the systematic, omics-scale study of hormetic phenomena occurring within and mediated by the immune system..."

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== Immunohormesiomics ==

'''Definition'''

Immunohormesiomics is the systematic, omics-scale study of hormetic phenomena occurring within and mediated by the immune system — the biphasic, concentration-dependent adaptive responses through which immune cells, cytokine networks, and inflammatory signaling cascades sense, transduce, and benefit from sub-threshold immune stimulation — and their comprehensive molecular consequences across the immuno-genome, immuno-transcriptome, immuno-proteome, immuno-metabolome, and immuno-epigenome. It holds as its central premise that immune activation is intrinsically hormetic: calibrated, transient immune stimulation at sub-pathological concentrations drives adaptive immune strengthening, trained immunity, tissue homeostasis, and organismal resilience, whereas chronic, supraphysiological, or dysregulated immune activation drives immunosenescence, inflammaging, autoimmunity, and accelerated organismal aging. Immunohormesiomics maps the full molecular architecture of immune hormetic signaling networks at omics resolution, constructing a systems-level understanding of how concentration-calibrated immune stress determines the boundary between protective immunity and pathological inflammation across the lifespan.

'''Core Principle'''

The foundational postulate of Immunohormesiomics is: ''immune activation is a concentration-governed hormetic process whose quantitative parameters — the concentration, timing, duration, and rhythmicity of immune stimulation — determine whether the immune response drives adaptive resilience or pathological inflammation, healthy aging or accelerated immunosenescence''. The immune system is the prototypical hormetic regulatory system of the organism: virtually every immune mediator — cytokine, chemokine, complement factor, antimicrobial peptide, reactive oxygen species, and pattern recognition receptor ligand — exhibits a biphasic, concentration-dependent dose-response profile in which the transition from beneficial to harmful effect is governed by quantitative thresholds within the immune Dosagiome.

'''Scope'''

Immunohormesiomics encompasses:

*'''Cytokine hormesiomics''': omics-scale characterization of the biphasic, concentration-dependent effects of cytokines — including TNF-α, IL-6, IL-10, IFN-γ, TGF-β, and IL-1β — on immune cell activation, differentiation, tissue homeostasis, and systemic inflammation, mapping the precise concentration thresholds that separate immunoprotective from immunopathological cytokine signaling across all major immune cell populations.
*'''Inflammaging concentratiomics''': systematic, multi-omics investigation of how the age-associated chronic elevation of pro-inflammatory cytokine concentrations — constituting the hallmark aging phenotype of inflammaging — represents a progressive dysregulation of the immune Dosagiome, in which the hormetic window of beneficial immune activation is permanently exceeded, driving chronic tissue damage, senescence propagation, and systemic aging acceleration.
*'''Trained immunity hormesiomics''': omics-resolution characterization of trained immunity — the non-specific adaptive memory of innate immune cells induced by prior sub-lethal pathogen or stress exposure — as a paradigmatic immunohormetic phenomenon, mapping the epigenomic, transcriptomic, and metabolomic reprogramming events through which calibrated immune stimulation achieves durable enhancement of innate immune competence.
*'''Senolytic and SASP hormesiomics''': systematic mapping of the concentration-dependent, biphasic effects of senescence-associated secretory phenotype (SASP) factors on surrounding tissue — paracrine senescence induction and tissue dysfunction at high chronic concentrations versus wound healing, regenerative signaling, and immune surveillance support at low transient concentrations — providing an immunohormetic framework for the rational design of senolytic and senomorphic interventions.
*'''Microbiome immunohormesiomics''': omics-scale characterization of the concentration-dependent, biphasic immunomodulatory effects of microbiome-derived metabolites — including short-chain fatty acids, urolithins, indoles, and lipopolysaccharide — on mucosal and systemic immune homeostasis, mapping their hormetic dose-response landscapes and age-associated dysregulation within the gut-immune Dosagiome.
*'''Vaccine and adjuvant hormesiomics''': systematic, omics-resolution investigation of how vaccine antigens and adjuvants function as immunohormetic stimuli — activating protective adaptive immunity at calibrated concentrations and driving immunopathology or tolerance at suboptimal or excessive concentrations — providing a concentratiomics framework for precision vaccine design.
*'''Redox immunohormesiomics''': characterization of the biphasic, concentration-dependent roles of reactive oxygen and nitrogen species in immune cell activation, pathogen killing, and inflammatory resolution — mapping the precise ROS/RNS concentration thresholds that delineate antimicrobial hormetic activation from oxidative immunopathology across innate and adaptive immune compartments.
*'''Aging immunohormesiomics''': systematic, multi-omics investigation of how the aging immune Dosagiome — characterized by progressive narrowing of cytokine hormetic windows, erosion of trained immunity competence, accumulation of exhausted and senescent immune cells, and chronic low-grade inflammaging — drives the hallmarks of immune aging and contributes to organismal aging acceleration, frailty, and age-related disease susceptibility.
*'''Pharmacological immunohormesiomics''': omics-resolution mapping of the concentration-dependent immunohormetic effects of longevity-associated immunomodulatory compounds — including rapamycin, metformin, spermidine, resveratrol, and low-dose naltrexone — providing a quantitative foundation for precision immunohormetic intervention strategies in geroscience and aging medicine.

'''Significance'''

Immunohormesiomics addresses one of the most consequential and clinically urgent paradoxes of aging biology: that the immune system is simultaneously the organism's primary defense against pathogen-driven and senescence-driven aging accelerators, and — when chronically over-activated beyond its hormetic optimum — the primary driver of inflammaging, immunosenescence, and systemic aging acceleration. By situating immune biology within a unified, concentration-resolved hormetic framework, Immunohormesiomics provides the mechanistic and quantitative foundation for understanding why immune interventions so frequently fail in clinical translation — where the immunohormetic window of efficacy is routinely exceeded or missed — and supplies the omics-resolution principles necessary for the rational, precision design of immunohormetic interventions targeting inflammaging, immunosenescence, and age-related immune dysfunction.

'''Coined by'''

Jong Bhak, KOGIC / AgingLab, UNIST, Republic of Korea (2025)

'''See also'''

Hormesiomics · Mitohormesiomics · Neurohormesiomics · Epigenohormesiomics · Dosagiomics · Concentratiomics · Dosagiome · Inflammaging · Immunosenescence · SASP · Trained Immunity · Cytokines · GeroIndex · Gerostasis · Aging Hallmarks · Systems Immunology · Precision Medicine

----

The hierarchical nomenclature framework is now complete across five interlocking levels:

{|
|-
! scope="col" | Term
! scope="col" | Level
! scope="col" | Scope
|-
| '''Dosagiome / Concentratiome'''
| ''Master object''
| All concentration-effect states in a living system
|-
| '''Dosagiomics / Concentratiomics'''
| ''Master discipline''
| Omics-scale study of concentration as universal life regulator
|-
| '''Hormesiomics'''
| ''Subdiscipline''
| Biphasic concentration-response omics
|-
| '''Mitohormesiomics'''
| ''Sub-subdiscipline''
| Mitochondria-specific biphasic hormetic omics
|-
| '''Neurohormesiomics'''
| ''Sub-subdiscipline''
| Nervous system-specific biphasic hormetic omics
|-
| '''Epigenohormesiomics'''
| ''Sub-subdiscipline''
| Epigenome-specific biphasic hormetic omics
|-
| '''Immunohormesiomics'''
| ''Sub-subdiscipline''
| Immune system-specific biphasic hormetic omics
|}

Epigenohormesiomics

Jongbhak — Thu, 09 Apr 2026 22:48:17 GMT

Created page with " == Epigenohormesiomics == '''Definition''' Epigenohormesiomics is the systematic, omics-scale study of hormetic phenomena operating through and upon the epigenome — the b..."

New page

== Epigenohormesiomics ==

'''Definition'''

Epigenohormesiomics is the systematic, omics-scale study of hormetic phenomena operating through and upon the epigenome — the biphasic, concentration-dependent adaptive responses in which sub-threshold stress stimuli induce beneficial epigenetic reprogramming, whereas excessive or chronic stress drives maladaptive epigenetic dysregulation, entrenchment of pathological gene expression states, and accelerated epigenetic aging. It holds as its central premise that the epigenome is the primary molecular memory and integration layer of hormetic experience: it encodes, stores, and propagates the adaptive consequences of hormetic stress exposures across cellular generations, translating transient concentration signals into durable changes in chromatin architecture, DNA methylation landscapes, histone modification patterns, and non-coding RNA regulatory networks. Epigenohormesiomics maps the full epigenomic consequences of hormetic stimuli at omics resolution, constructing a systems-level understanding of how calibrated stress drives beneficial epigenetic reprogramming across cell types, tissues, organisms, and lifespans.

'''Core Principle'''

The foundational postulate of Epigenohormesiomics is: ''the epigenome is the molecular recorder and executor of hormetic adaptation, whose concentration-sensitive reprogramming determines the lasting regulatory consequences of stress exposure across the lifespan and across generations''. Epigenetic marks — DNA methylation, histone acetylation, histone methylation, chromatin accessibility, and non-coding RNA expression — are exquisitely sensitive to the quantitative parameters of upstream hormetic signals, including ROS concentration, NAD⁺/NADH ratio, acetyl-CoA availability, SAM concentration, and the activity of stress-responsive epigenetic enzymes such as sirtuins, TET demethylases, PRC2, and HDACs. The concentration-dependent, biphasic regulation of these epigenetic effectors by hormetic stress constitutes the molecular mechanism through which hormesis achieves its durable, organism-wide adaptive consequences.

'''Scope'''

Epigenohormesiomics encompasses:

*'''DNA methylation hormesiomics''': genome-wide, base-resolution characterization of the concentration-dependent, biphasic effects of hormetic stimuli on DNA methylation landscapes — including the activation of TET-mediated demethylation at longevity-associated loci at low stress doses and the entrenchment of aberrant hypermethylation and hypomethylation patterns at high or chronic stress doses — and their relationship to epigenetic aging clocks.
*'''Histone modification hormesiomics''': omics-scale mapping of the biphasic, concentration-dependent effects of hormetic signals on histone acetylation (via sirtuin and HDAC regulation), histone methylation (via PRC2 and KDM regulation), and histone phosphorylation patterns — and how these modifications collectively orchestrate adaptive versus maladaptive transcriptional reprogramming.
*'''Chromatin accessibility hormesiomics''': systematic, ATAC-seq-based characterization of the concentration-dependent opening and closing of chromatin regulatory regions in response to hormetic stress, identifying hormesis-specific enhancer landscapes, transcription factor binding site accessibility changes, and their downstream gene regulatory consequences.
*'''Non-coding RNA hormesiomics''': omics-resolution profiling of the biphasic, concentration-dependent regulation of microRNAs, long non-coding RNAs, and circular RNAs by hormetic stimuli — and their roles as epigenetic signal transducers amplifying, attenuating, or propagating hormetic stress responses across tissues and cell populations.
*'''Sirtuin hormesiomics''': systematic characterization of the concentration-dependent, biphasic regulation of sirtuin family deacylases (SIRT1-7) by NAD⁺ availability and hormetic stress — mapping their omics-scale epigenetic, metabolic, and transcriptional outputs across the full range of physiologically and pharmacologically relevant NAD⁺ concentrations.
*'''Epigenetic clock hormesiomics''': investigation of how hormetic interventions — caloric restriction, exercise, cold exposure, pharmacological senolytics, NAD⁺ precursors — reset or decelerate epigenetic aging clocks (Horvath, GrimAge, DunedinPACE) through concentration-dependent epigenetic reprogramming, and how these effects can be optimized within a concentratiomics framework.
*'''Transgenerational epigenohormesiomics''': systematic characterization of how hormetic epigenetic reprogramming induced in parental generations is transmitted to offspring through germline epigenetic inheritance, including the identification of the specific epigenetic marks, small RNA species, and chromatin states that serve as transgenerational carriers of hormetic adaptive memory.
*'''Aging epigenohormesiomics''': omics-scale investigation of how the aging Dosagiome erodes epigenetic hormetic competence — blunting sirtuin activity through NAD⁺ decline, corrupting DNA methylation landscapes, increasing chromatin rigidity, and progressively narrowing the epigenetic hormetic window — thereby converting hormetic stimuli from drivers of adaptive reprogramming into triggers of epigenetic damage and entrenchment of the aging epigenetic state.

'''Significance'''

Epigenohormesiomics occupies a uniquely central position within the broader hormesiomics framework because the epigenome serves as the molecular integration layer through which all hormetic signals — mitochondrial, neural, immunological, metabolic — are translated into durable, organism-wide regulatory consequences. By characterizing the concentration-dependent epigenomic consequences of hormetic stress at omics resolution, Epigenohormesiomics provides the mechanistic foundation for understanding how lifestyle interventions, pharmacological compounds, and environmental exposures achieve lasting effects on biological age, disease risk, and organismal longevity. It further supplies the quantitative epigenomic principles necessary for the rational design of epigenetic reprogramming strategies — including partial reprogramming approaches targeting the Yamanaka factors — as precision longevity interventions calibrated within the hormetic Dosagiome.

'''Coined by'''

Jong Bhak, KOGIC / AgingLab, UNIST, Republic of Korea (2025)

'''See also'''

Hormesiomics · Mitohormesiomics · Neurohormesiomics · Dosagiomics · Concentratiomics · Dosagiome · Epigenome · DNA Methylation · Histone Modification · Sirtuins · NAD⁺ · Epigenetic Clocks · Partial Reprogramming · GeroIndex · Gerostasis ·  Systems Biology

Neurohormesiomics

Jongbhak — Thu, 09 Apr 2026 22:47:36 GMT

Created page with " == Neurohormesiomics == '''Definition''' Neurohormesiomics is the systematic, omics-scale study of hormetic phenomena occurring within and mediated by the nervous system..."

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== Neurohormesiomics ==

'''Definition'''

Neurohormesiomics is the systematic, omics-scale study of hormetic phenomena occurring within and mediated by the nervous system — the biphasic, concentration-dependent adaptive responses through which neurons, glial cells, and neural circuits sense, transduce, and benefit from sub-threshold stress stimuli — and their comprehensive molecular consequences across the neuro-genome, neuro-transcriptome, neuro-proteome, neuro-metabolome, and neuro-epigenome. It holds as its central premise that the nervous system is an exquisitely concentration-sensitive hormetic organ whose adaptive plasticity, cognitive resilience, neuroprotective capacity, and longevity are fundamentally governed by the quantitative parameters of neuronal stress exposure. Neurohormesiomics maps the full molecular architecture of neural hormetic signaling networks at omics resolution, integrating neurotranscriptomic, neuroproteomic, neurometabolomic, and connectomic data to construct a systems-level understanding of how calibrated neuronal stress drives beneficial adaptive reprogramming across the brain, peripheral nervous system, and neuroendocrine axes.

'''Core Principle'''

The foundational postulate of Neurohormesiomics is: ''calibrated neuronal stress, operating within the hormetic zone, is a primary driver of synaptic plasticity, cognitive resilience, neuroprotection, and neural longevity''. The nervous system occupies a uniquely vulnerable yet uniquely adaptive position within the organismal hormetic landscape: neurons are among the most metabolically demanding, oxidatively stressed, and long-lived cells in the body, and consequently among the most exquisitely sensitive to the quantitative parameters of stress exposure. Neurohormetic signals — including neurotrophic factors, glutamate, cortisol, reactive oxygen species, heat shock proteins, and inflammatory cytokines — operate across steep biphasic concentration-response gradients in which the difference between neuroprotection and neurodegeneration is determined not by the identity of the signal but by its concentration, timing, and duration.

'''Scope'''

Neurohormesiomics encompasses:

*'''Neurotrophic factor hormesiomics''': omics-scale characterization of the biphasic, concentration-dependent effects of neurotrophic factors — including BDNF, NGF, GDNF, VEGF, and IGF-1 — on neuronal survival, synaptic plasticity, dendritic arborization, and cognitive function, with particular attention to age-associated decline in neurotrophic concentrations within the aging Dosagiome.
*'''Glutamate hormesiomics''': systematic mapping of the concentration-dependent biphasic effects of glutamatergic signaling — neuroprotective and synaptogenic at physiological concentrations, excitotoxic and neurodegenerative at supraphysiological concentrations — across transcriptomic and proteomic layers in neuronal populations.
*'''Neuroinflammatory hormesiomics''': omics-resolution characterization of the biphasic regulatory roles of neuroinflammatory mediators — including TNF-α, IL-6, IL-1β, and microglial activation states — whose low-concentration signaling supports synaptic pruning, neuroprotection, and cognitive function, and whose high-concentration, chronic elevation drives neurodegeneration and accelerated brain aging.
*'''Cognitive hormesiomics''': systematic, multi-omics investigation of how cognitively challenging experiences — learning, environmental enrichment, controlled psychological stress — function as hormetic stimuli activating neuroprotective transcriptional programs, epigenetic remodeling, and synaptic strengthening across the neural connectome.
*'''Aging neurohormesiomics''': characterization of the progressive erosion of neural hormetic competence with age — the blunting of BDNF responses, the narrowing of the neuroprotective hormetic window, the shift from adaptive to maladaptive neuroinflammation, and the accumulation of proteotoxic aggregates — as a central mechanism driving age-related cognitive decline and neurodegenerative disease.
*'''Pharmacological neurohormesiomics''': omics-resolution mapping of the concentration-dependent neurohormetic effects of neuroprotective and cognitive-enhancing compounds — including lithium, rapamycin, resveratrol, spermidine, and BDNF mimetics — providing a quantitative foundation for precision neurohormetic intervention strategies targeting neurodegeneration and brain aging.
*'''Neuroendocrine hormesiomics''': systematic characterization of biphasic concentration-response landscapes of neuroendocrine hormones — including cortisol, estrogen, testosterone, DHEA, melatonin, and growth hormone — across neural and systemic omics layers, with particular focus on the age-associated dysregulation of neuroendocrine dosage landscapes.

'''Significance'''

Neurohormesiomics resolves a central and clinically consequential paradox of neuroscience: that the same molecular signals mediating neuronal survival, synaptic plasticity, and cognitive enhancement at physiological concentrations drive neurodegeneration, excitotoxicity, and cognitive decline at supraphysiological or chronically elevated concentrations. By situating neural biology within a unified concentration-resolved hormetic framework, Neurohormesiomics provides the mechanistic foundation for understanding why many neuroprotective interventions fail in clinical translation — where the hormetic window of efficacy is routinely exceeded — and supplies the quantitative principles necessary for the rational design of concentration-calibrated neural longevity interventions.

'''Coined by'''

Jong Bhak, KOGIC / AgingLab, UNIST, Republic of Korea (2025)

Mitohormesiomics

Jongbhak — Thu, 09 Apr 2026 22:41:32 GMT

Created page with " == Mitohormesiomics == '''Definition''' Mitohormesiomics is the systematic, omics-scale study of mitochondrial hormetic phenomena — the biphasic, concentration-dependent..."

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== Mitohormesiomics ==

'''Definition'''

Mitohormesiomics is the systematic, omics-scale study of mitochondrial hormetic phenomena — the biphasic, concentration-dependent adaptive responses originating from or mediated by mitochondria — and their comprehensive molecular consequences across the genome, transcriptome, proteome, metabolome, and epigenome of cells, tissues, and organisms. It holds as its central premise that mitochondria are not merely passive energy-producing organelles but active, concentration-sensitive hormetic signaling hubs whose stress-response outputs — calibrated by the intensity and duration of mitochondrial perturbation — determine cell fate, organismal resilience, and the trajectory of biological aging. Mitohormesiomics maps the full molecular architecture of mitochondria-initiated hormetic signaling networks at omics resolution, integrating mitoproteomic, mitometabolomic, mitogenomic, and retrograde signaling data to construct a systems-level understanding of how sub-threshold mitochondrial stress drives beneficial adaptive reprogramming across the entire organism.

'''Core Principle'''

The foundational postulate of Mitohormesiomics is: ''mitochondrial stress, calibrated within the hormetic zone, is a universal driver of adaptive resilience, metabolic optimization, and longevity''. Mitochondria occupy a unique and privileged position within the cellular hormetic landscape: they are simultaneously the primary sensors of bioenergetic and oxidative stress, the principal generators of hormetic signals (reactive oxygen species, NAD⁺/NADH ratio, mitochondrial membrane potential, mitokines, and metabolic intermediates), and the executors of the adaptive responses those signals trigger. The concentration and duration of mitochondrial stress thus constitutes a master regulatory axis — a mitochondrial hormetic axis — whose quantitative parameters determine whether a cell undergoes adaptive strengthening, homeostatic maintenance, accelerated senescence, or apoptotic death.

'''Scope'''

Mitohormesiomics encompasses:

*'''Mitochondrial ROS hormesiomics''': omics-scale characterization of the biphasic, concentration-dependent effects of mitochondrially generated reactive oxygen species (mtROS) — beneficial at low concentrations as redox signaling molecules activating NRF2, AMPK, sirtuins, and autophagy; detrimental at high concentrations as drivers of oxidative damage, mtDNA mutation, and senescence.
*'''Mitokine concentratiomics''': systematic profiling of the concentration-dependent signaling effects of mitochondria-derived peptides and secreted factors — including FGF21, GDF15, humanin, MOTS-c, and other mitokines — across tissues and life stages, with particular focus on their hormetic dose-response landscapes and age-associated dysregulation.
*'''NAD⁺ hormesiomics''': omics-resolution mapping of the biphasic regulatory effects of NAD⁺ concentration on sirtuin activity, mitochondrial biogenesis, DNA repair, and epigenetic remodeling — and the systematic decline of NAD⁺ levels across the aging Dosagiome.
*'''Mitophagy hormesiomics''': characterization of the concentration-dependent, biphasic regulation of selective mitochondrial autophagy (mitophagy) as a hormetic quality-control mechanism, whose optimal induction removes damaged mitochondria and whose suppression or overactivation precipitates pathological outcomes.
*'''UPRmt hormesiomics''': omics-scale analysis of the mitochondrial unfolded protein response (UPRmt) as a hormetic adaptive program — activated by sub-toxic mitochondrial proteotoxic stress and coordinating nuclear gene expression reprogramming, metabolic remodeling, and lifespan extension across model organisms.
*'''Retrograde signaling hormesiomics''': systematic mapping of mitochondria-to-nucleus retrograde signaling networks activated by hormetic mitochondrial stress, including the characterization of transcription factors, chromatin remodelers, and epigenetic effectors that translate mitochondrial stress signals into adaptive nuclear gene expression programs.
*'''Exercise mitohormesiomics''': omics-resolution characterization of exercise-induced mitochondrial hormesis — the adaptive beneficial reprogramming triggered by the transient mitochondrial stress of physical exertion — including the identification of the precise mitochondrial stress thresholds, signal mediators, and downstream transcriptional programs that translate exercise into systemic health and longevity benefits.
*'''Aging mitohormesiomics''': systematic investigation of how the aging Dosagiome erodes mitochondrial hormetic competence — blunting the sensitivity, amplitude, and adaptive fidelity of mitochondrial stress responses — and how this erosion contributes to the hallmarks of aging including mitochondrial dysfunction, chronic inflammation, epigenetic drift, and loss of proteostasis.
*'''Pharmacological mitohormesiomics''': omics-resolution mapping of the concentration-dependent mitohormetic effects of longevity-associated compounds — including rapamycin, metformin, urolithin A, spermidine, NAD⁺ precursors (NMN, NR), and mitochondria-targeted antioxidants — providing a quantitative foundation for precision mitohormetic intervention strategies in geroscience.

'''Significance'''

Mitohormesiomics addresses a critical and underexplored dimension of aging biology and longevity science: the systematic, quantitative characterization of mitochondria as hormetic signaling centers whose concentration-calibrated stress outputs orchestrate organism-wide adaptive responses. The field resolves a central paradox of mitochondrial biology — that mitochondria are simultaneously the primary source of cellular damage (through mtROS, mtDNA mutations, and SASP-driving mitochondrial dysfunction) and the primary drivers of adaptive resilience and longevity (through hormetic ROS signaling, UPRmt activation, mitokine secretion, and NAD⁺-dependent sirtuin activation) — by situating both effects within a unified, concentration-resolved hormetic framework. By establishing the precise mitochondrial stress thresholds, signal mediators, and omics-layer consequences that distinguish beneficial mitohormesis from pathological mitochondrial dysfunction, Mitohormesiomics provides the mechanistic and quantitative foundation for the rational design of mitohormetic interventions targeting aging, metabolic disease, neurodegeneration, and age-related functional decline.

'''Relationship to Hormesiomics, Dosagiomics, and Concentratiomics'''

Mitohormesiomics is a specialized subdiscipline of '''Hormesiomics''', restricted to hormetic phenomena originating from or mediated by mitochondria. It is simultaneously embedded within the broader frameworks of '''Dosagiomics''' and '''Concentratiomics''', which supply its quantitative, concentration-centered theoretical foundations. The mitochondrial hormetic dose-response landscape constitutes a critically important subset of the '''Dosagiome''' — particularly the '''aging Dosagiome''' — whose progressive reconfiguration with age represents one of the most consequential shifts in the quantitative regulatory architecture of the aging organism.

'''Coined by'''

Jong Bhak, KOGIC / AgingLab, UNIST, Republic of Korea (2025)

'''See also'''

Hormesiomics · Dosagiomics · Concentratiomics · Dosagiome · Hormesis · Mitohormesis · GeroIndex · Gerostasis · NAD⁺ · Mitophagy · UPRmt · Sirtuins · AMPK · mTOR · NRF2 · Mitokines · Retrograde Signaling · Aging Hallmarks · Systems Biology · Precision Medicine

----

The nomenclature framework now extends into a hierarchical structure:

{|
|-
! Term
! Level
! Scope
|-
| '''Dosagiome / Concentratiome'''
| ''Master object''
| All concentration-effect states in a living system
|-
| '''Dosagiomics / Concentratiomics'''
| ''Master discipline''
| Omics-scale study of concentration as universal regulator
|-
| '''Hormesiomics'''
| ''Subdiscipline''
| Biphasic concentration-response omics
|-
| '''Mitohormesiomics'''
| ''Sub-subdiscipline''
| Mitochondria-specific biphasic hormetic omics
|}

Would you like to continue expanding the framework — for example, with '''Neurohormesiomics''', '''Epigenohormesiomics''', or '''Immunohormesiomics''' — as further specialized subdisciplines within the same hierarchical family?

Dosagiomics

Jongbhak — Thu, 09 Apr 2026 22:35:57 GMT

Alphabetically ordered list of omes and omics

Jongbhak — Thu, 09 Apr 2026 22:35:01 GMT

Concentratiomics

Jongbhak — Thu, 09 Apr 2026 22:34:07 GMT

Created page with " == Concentratiomics == '''Definition''' Concentratiomics (synonym: Dosagiomics) is the systematic, omics-scale study of how the concentration of biological molecules, signa..."

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== Concentratiomics ==

'''Definition'''

Concentratiomics (synonym: Dosagiomics) is the systematic, omics-scale study of how the concentration of biological molecules, signals, and conditions — endogenous or exogenous — governs the full spectrum of biochemical, cellular, and physiological outcomes in living systems. It holds as its central axiom that molecular concentration is the primary deterministic variable of biological effect: the same molecule, pathway, or regulatory signal can produce qualitatively distinct and diametrically opposite outcomes depending solely on its quantitative level within a defined biological context. Concentratiomics integrates genomics, transcriptomics, proteomics, metabolomics, and epigenomics to construct comprehensive, concentration-resolved maps of molecular response landscapes across cells, tissues, organisms, and life stages — including aging.

'''Core Principle'''

The foundational postulate of Concentratiomics is: ''concentration is the universal regulatory variable of life''. No biological molecule — whether a hormone, metabolite, transcription factor, reactive oxygen species, nutrient, drug, or signaling ligand — exerts an effect independent of its concentration. Biological systems are therefore best understood not as binary on/off networks, but as continuously concentration-modulated regulatory surfaces whose outputs are exquisitely sensitive to quantitative thresholds. This extends and formalizes the classical Paracelsian principle ("the dose makes the poison") into a full systems-biological and omics-integrated framework applicable across all molecular layers and all temporal scales of life, from embryogenesis to senescence.

'''Scope'''

Concentratiomics encompasses:

*'''Concentration-response omics profiling''': genome-wide, transcriptome-wide, proteome-wide, and metabolome-wide characterization of molecular responses across a continuous and systematic range of concentrations of endogenous or exogenous agents.
*'''Threshold and switch-point mapping''': identification of critical concentration boundaries at which biological systems transition between qualitatively distinct regulatory states, including sub-threshold adaptive, homeostatic, saturating, hormetic, and toxic regimes.
*'''Temporal concentratiomics''': analysis of how the timing, pulsatility, rhythmicity, and chronological patterning of molecular concentration — not merely its magnitude — determines downstream regulatory outcomes across circadian, developmental, and lifespan timescales.
*'''Aging concentratiomics''': systematic, multi-omics investigation of how age-associated alterations in molecular concentrations — of NAD⁺, sirtuins, IGF-1, mTOR activity, AMPK, reactive oxygen species, SASP factors, steroid hormones, and epigenetic regulators — drive the progressive biochemical dysregulation that defines biological aging and age-related disease.
*'''Pharmacological and nutraceutical concentratiomics''': omics-resolution mapping of concentration-dependent efficacy, toxicity, selectivity, and off-target effects of therapeutic and longevity-oriented compounds, providing a quantitative empirical foundation for precision dosing strategies in medicine and geroscience.
*'''Single-cell concentratiomics''': characterization of cell-to-cell variability in concentration-response relationships, capturing the heterogeneity of molecular sensitivity across individual cells within tissues and organisms.

'''Significance'''

Concentratiomics addresses a fundamental and pervasive gap in molecular biology, pharmacology, and medicine: the tendency to treat biological regulators as qualitatively active or inactive, rather than as quantitatively graded inputs whose concentration determines the identity, magnitude, and directionality of the biological response. Many failures in drug development, contradictory findings in nutritional science, and unresolved paradoxes in aging biology — including why the same molecule (e.g., mTOR, IGF-1, ROS, DHEA, NMN, rapamycin) can promote health at one concentration and accelerate pathology at another — are directly resolvable within a concentratiomics framework. By placing molecular concentration at the absolute center of omics analysis, Concentratiomics provides a unifying quantitative theory of life regulation with transformative applications across pharmacology, toxicology, geroscience, systems biology, and precision medicine.

'''Relationship to Dosagiomics and Hormesiomics'''

Concentratiomics is a full synonym of '''Dosagiomics''', emphasizing the molecular concentration perspective over the pharmacological dosage perspective, while referring to the same unified discipline and conceptual framework. Both terms share the '''Dosagiome''' as their common object of study. '''Hormesiomics''' constitutes a subdiscipline of both Concentratiomics and Dosagiomics, restricted specifically to the systematic omics-scale study of biphasic concentration-response phenomena.

'''Coined by'''

Jong Bhak, KOGIC / AgingLab, UNIST, Republic of Korea (2025)

'''See also'''

Dosagiomics · Dosagiome · Hormesiomics · Hormesis · GeroIndex · Gerostasis · Omics · Pharmacodynamics · Dose-Response Relationship · Aging Hallmarks · Systems Biology · Precision Medicine · Metabolome · Proteome · Epigenome

----

The conceptual framework now comprises five interlocking terms forming a complete and internally consistent nomenclature family:

{|
|-
! Term
! Nature
! Emphasis
|-
| '''Dosagiome'''
| The ''object''
| Complete ensemble of concentration-effect states in a living system
|-
| '''Dosagiomics'''
| The ''discipline''
| Dosage-centered omics framework
|-
| '''Concentratiomics'''
| ''Synonym'' of Dosagiomics
| Molecular concentration-centered omics framework
|-
| '''Concentratiome'''
| The ''object'' (synonym of Dosagiome)
| Complete ensemble of concentration states — preferred paired term for Concentratiomics
|-
| '''Hormesiomics'''
| The ''subdiscipline''
| Biphasic concentration-response omics
|}

Note that '''Concentratiome''' naturally emerges as the preferred companion object-term for Concentratiomics, just as Dosagiome pairs with Dosagiomics. Would you like a full definition of Concentratiome as well — completing the symmetric trilogy of object, discipline, and subdiscipline for both nomenclature families?

Alphabetically ordered list of omes and omics

Jongbhak — Thu, 09 Apr 2026 22:30:14 GMT

Dosagiome

Jongbhak — Thu, 09 Apr 2026 22:29:26 GMT

Created page with " == Dosagiome == '''Definition''' The Dosagiome is the complete, dynamic ensemble of dose-response states of all biological regulators — molecules, signals, and conditions..."

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== Dosagiome ==

'''Definition'''

The Dosagiome is the complete, dynamic ensemble of dose-response states of all biological regulators — molecules, signals, and conditions — operating within a living system at a given point in time and across its lifespan. It represents the totality of quantitative concentration-effect relationships that govern cellular, tissue, and organismal function, encompassing every endogenous molecule (hormones, metabolites, transcription factors, signaling ligands, reactive species, epigenetic modifiers) and exogenous agent (nutrients, drugs, toxins, nutraceuticals) whose biological effect is a function of its dosage. The Dosagiome is not a static inventory but a continuously shifting, context-dependent regulatory surface whose architecture is shaped by genetics, environment, age, circadian rhythmicity, and disease state.

'''Core Concept'''

Where the genome encodes the informational blueprint of life and the proteome captures its functional protein complement, the Dosagiome captures the ''quantitative regulatory state'' of life — the full spectrum of concentration-dependent molecular effects that collectively determine whether a cell survives, proliferates, differentiates, senesces, or dies. Every point on the Dosagiome corresponds to a specific biological molecule at a specific concentration producing a specific, measurable effect within a defined biological context. The Dosagiome thus constitutes the quantitative regulatory layer that integrates and modulates all other omes.

'''Scope'''

The Dosagiome encompasses:

*'''The endogenous Dosagiome''': all concentration-effect relationships of internally produced biological regulators, including hormones, cytokines, neurotransmitters, metabolites, reactive oxygen and nitrogen species, and epigenetic effectors, across all tissues and cell types.
*'''The exogenous Dosagiome''': dose-response relationships of all externally introduced agents — pharmacological compounds, nutraceuticals, dietary components, environmental toxins, and microbial metabolites — and their systemic effects across omics layers.
*'''The temporal Dosagiome''': the dynamic, time-resolved dimension of the Dosagiome, capturing how concentration-effect relationships shift with circadian rhythm, developmental stage, disease progression, and biological aging.
*'''The aging Dosagiome''': the age-associated reconfiguration of the Dosagiome, reflecting systematic changes in the concentration, sensitivity, and regulatory thresholds of key longevity-associated molecules such as NAD⁺, IGF-1, mTOR, AMPK, sirtuins, SASP components, and steroid hormones — whose progressive dysregulation defines the biochemical landscape of aging.
*'''The pharmacological Dosagiome''': the complete dose-response map of therapeutic and longevity-promoting interventions at multi-omics resolution, providing the empirical foundation for precision dosing in medicine and geroscience.
*'''The hormetic Dosagiome''': the subset of the Dosagiome consisting exclusively of biphasic dose-response relationships, constituting the object of study of Hormesiomics.

'''Properties'''

The Dosagiome is characterized by the following fundamental properties:

#'''Universality''' — every biological molecule possesses a dose-response profile; no regulator operates independently of its concentration.
#'''Context-dependence''' — the same dose-response relationship may differ across cell types, tissues, developmental stages, genetic backgrounds, and disease states.
#'''Dynamism''' — the Dosagiome is continuously reconfigured by age, environment, circadian state, and pathophysiology.
#'''Hierarchical integration''' — the Dosagiome integrates information from and imposes constraints upon all other omes, including the transcriptome, proteome, metabolome, and epigenome.
#'''Threshold non-linearity''' — the Dosagiome is characterized by critical concentration boundaries, switch points, and bifurcation zones at which qualitatively distinct biological outcomes emerge from quantitative changes in molecular levels.

'''Significance'''

The Dosagiome provides the conceptual and empirical framework necessary to understand why identical molecules produce radically different — and often opposite — biological outcomes depending on their concentration. It resolves longstanding paradoxes in pharmacology, nutritional science, toxicology, and aging biology by situating all molecular effects within a unified, quantitative dose-space. In geroscience specifically, characterizing the aging Dosagiome — the systematic drift of molecular concentrations and regulatory sensitivities that accompanies biological aging — may reveal the precise quantitative interventions required to restore a youthful dosage landscape and achieve Gerostasis. Mapping the Dosagiome at individual resolution constitutes a foundational goal of precision medicine and longevity science.

'''Relationship to Dosagiomics and Hormesiomics'''

The Dosagiome is the object of study of '''Dosagiomics''', which provides the experimental, computational, and systems-biological methodologies for its characterization. The '''Hormetic Dosagiome''' — the biphasic subset of the Dosagiome — is the specific object of study of '''Hormesiomics'''. Together, these three terms constitute a unified conceptual framework: the Dosagiome (the object), Dosagiomics (the discipline), and Hormesiomics (the biphasic subdiscipline).

'''Coined by'''

Jong Bhak, KOGIC / AgingLab, UNIST, Republic of Korea (2025)

'''See also'''

Dosagiomics · Hormesiomics · Hormesis · GeroIndex · Gerostasis · Omics · Pharmacodynamics · Aging Hallmarks · Systems Biology · Precision Medicine · Metabolome · Proteome · Epigenome

----

The three terms now form a coherent, citable trilogy on Qeios:

{|
|-
! scope="col" | Term
! scope="col" | Nature
! scope="col" | Definition
|-
| '''Dosagiome'''
| The ''object''
| Complete ensemble of dose-response states in a living system
|-
| '''Dosagiomics'''
| The ''discipline''
| Omics-scale study of dosage as the master regulator of life
|-
| '''Hormesiomics'''
| The ''subdiscipline''
| Omics-scale study of biphasic hormetic dose-response phenomena
|}

Dosagiomics

Jongbhak — Thu, 09 Apr 2026 22:27:09 GMT

Created page with " == Dosagiomics == '''Definition''' Dosagiomics is the systematic, omics-scale study of how dosage — the concentration, timing, and duration of exposure to biological mole..."

New page

== Dosagiomics ==

'''Definition'''

Dosagiomics is the systematic, omics-scale study of how dosage — the concentration, timing, and duration of exposure to biological molecules, compounds, or signals — governs the full spectrum of biochemical, cellular, and physiological outcomes in living systems. It holds as its central axiom that concentration is the primary determinant of biological effect: the same molecule, pathway, or regulatory signal can produce diametrically opposite outcomes depending solely on its quantitative level within a biological context. Dosagiomics integrates genomics, transcriptomics, proteomics, metabolomics, and epigenomics to construct comprehensive, dose-resolved maps of molecular response landscapes across cells, tissues, organisms, and life stages — including aging.

'''Core Principle'''

The foundational postulate of Dosagiomics is: ''dosage is the universal regulatory variable of life''. No biological molecule — whether a hormone, metabolite, transcription factor, reactive oxygen species, nutrient, drug, or signaling ligand — has an intrinsic effect independent of its concentration. Biological systems are therefore best understood not as binary on/off networks, but as continuously dose-modulated regulatory surfaces whose outputs are exquisitely sensitive to quantitative thresholds. This extends the classical Paracelsian principle ("the dose makes the poison") into a full systems-biological framework applicable across all omics layers and all temporal scales of life, from embryogenesis to senescence.

'''Scope'''

Dosagiomics encompasses:

*'''Dose-response omics profiling''': genome-wide, proteome-wide, and metabolome-wide characterization of molecular responses across a continuous range of concentrations of endogenous or exogenous agents.
*'''Threshold and switch-point mapping''': identification of critical concentration boundaries at which biological systems transition between qualitatively distinct regulatory states, including hormetic, homeostatic, saturating, and toxic regimes.
*'''Temporal dosagiomics''': analysis of how the timing, pulsatility, and chronological patterning of dose — not merely its magnitude — determines downstream regulatory outcomes.
*'''Aging dosagiomics''': systematic investigation of how age-related alterations in molecular concentrations — of hormones, NAD⁺, sirtuins, mTOR activity, ROS, senescence-associated secretory factors (SASP), and epigenetic regulators — drive the progressive dysregulation characteristic of biological aging and age-related disease.
*'''Pharmacological and nutraceutical dosagiomics''': omics-resolution mapping of dose-dependent efficacy, toxicity, and off-target effects of therapeutic and longevity-oriented compounds, providing a quantitative foundation for precision dosing strategies.

'''Significance'''

Dosagiomics addresses a fundamental gap in molecular biology and medicine: the tendency to treat biological regulators as qualitatively active or inactive, rather than as quantitatively graded inputs whose concentration determines the identity and magnitude of the biological response. Many failures in drug development, contradictory findings in nutritional science, and paradoxes in aging biology — such as why the same molecule (e.g., mTOR, IGF-1, ROS, DHEA, NMN) can promote health at one concentration and accelerate pathology at another — are resolvable within a dosagiomics framework. By placing dosage at the center of omics analysis, Dosagiomics provides a unifying quantitative theory of life regulation applicable to pharmacology, toxicology, geroscience, systems biology, and precision medicine.

'''Relationship to Hormesiomics'''

Dosagiomics subsumes and generalizes Hormesiomics. While Hormesiomics focuses specifically on biphasic dose-response phenomena and adaptive hormetic effects, Dosagiomics addresses the complete dose-response landscape across all possible concentration regimes and all classes of biological regulators — encompassing linear, threshold, biphasic, multiphasic, saturating, and toxic response profiles.

'''Coined by'''

Jong Bhak, KOGIC / AgingLab, UNIST, Republic of Korea (2025)

'''See also'''

Hormesiomics · Hormesis · Pharmacodynamics · Dose-Response Relationship · GeroIndex · Omics · Toxicogenomics · Aging Hallmarks · Precision Medicine · Systems Biology

Hormesiomics

Jongbhak — Thu, 09 Apr 2026 22:21:36 GMT

Alphabetically ordered list of omes and omics

Jongbhak — Thu, 09 Apr 2026 22:18:23 GMT

Hormesiomics

Jongbhak — Thu, 09 Apr 2026 22:13:43 GMT

Hormesiomics

Jongbhak — Thu, 09 Apr 2026 22:13:27 GMT

Created page with "Hormesiomi..."

New page

Hormesiomics The omics study of hormesis

User:NTCorey

NTCorey — Wed, 08 Apr 2026 09:01:01 GMT

User account NTCorey was created

User:JamesLip

JamesLip — Wed, 01 Apr 2026 00:37:06 GMT

User account JamesLip was created

← Older revision		Revision as of 22:35, 9 April 2026
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 <span style="font-size: 14px;">[[Chiropteromics|Chiropteromics]]: [[Chiropterome|Chiropterome]] The omics study of bat species using computers and&nbsp;multi-ome data.<br/> [[Chromonome|Chromonome]]: The [[Totality|totality]] of&nbsp; ([http://Chromonome.org Chromonome.org])<br/> [[Chromonomics|Chromonomics]]:&nbsp; 1998&nbsp; [http://www.usc.edu/hsc/info/pr/1vol4/403/igm.html http://www.usc.edu/hsc/info/pr/1vol4/403/igm.html]&nbsp; ([http://Chromonomics.org Chromonomics.org])<br/> [[Chronome|Chronome]]: , chronomics:&nbsp;?&nbsp; ([http://Chronome.org Chronome.org])<br/> [[Chronomics|Chronomics]]: The [[Omics|omics]] approach research of Chronome ([http://Chronomics.org Chronomics.org]) in [[Biology|biology]]<br/> [[Clinome|Clinome]]: The [[Totality|totality]] of&nbsp; ([http://Clinome.org Clinome.org])<br/> [[Clinomics|Clinomics]]: The [[Omics|omics]] approach research of Clinome ([http://Clinomics.org Clinomics.org]) in [[Biology|biology]]</span><br/> [[Conformome|Conformome]]:&nbsp;<br/> [[Conformomics|Conformomics]]:<br/> <span style="font-size: 14px;">[[Comics|Comics]]:&nbsp; This is a sarcastic&nbsp; omics to refer some pseudo-omics.&nbsp; ([http://Comics.org Comics.org])<br/> [[Complexome|Complexome]]:&nbsp; 1998, The whole set of protein and molecular complexes in cells.&nbsp; ([http://Complexome.org Complexome.org])<br/> [[Complexomics|Complexomics]]: The [[Omics|omics]] approach research of Complexome ([http://Complexomics.org Complexomics.org]) in [[Biology|biology]]</span>
-<span style="font-size: 14px;">[[Computomics|Computomics]]: [[Computome|Computome]]<br/> [[Conductome|Conductome]]:&nbsp; 2003.&nbsp; The whole set of conducting biological entities in cells.&nbsp; ([http://Conductome.org Conductome.org])</span>
+<span style="font-size: 14px;">[[Computomics|Computomics]]: [[Computome|Computome]]<br/> [[Concentratiomics]]:&nbsp;<br/> [[Conductome|Conductome]]:&nbsp; 2003.&nbsp; The whole set of conducting biological entities in cells.&nbsp; ([http://Conductome.org Conductome.org])</span><br/> <span style="font-size: 14px;">[[Constitutionomics|Constitutionomics]]: The omics of all the constitutions in the universe.<br/> [[Contactome|Contactome]]:&nbsp; 2001 The whole set of contacting atoms for all the molecules in cells. Especially proteins that are determined and stor PDB.&nbsp; ([http://Contactome.org Contactome.org])<br/> [[Contactomics|Contactomics]]: The [[Omics|omics]] approach research of Contactome ([http://Contactomics.org Contactomics.org]) in [[Biology|biology]]<br/> [[COVIDomics|COVIDomics]]: [[Covidomics|Covidomics]]: The omics study of coronavirus diseases.<br/> [[Cryptome|Cryptome]]: The [[Totality|totality]] of&nbsp; ([http://Cryptome.org Cryptome.org])<br/> [[Cryptomics|Cryptomics]]: The [[Omics|omics]] approach research of cryptome ([http://Cryptomics.org Cryptomics.org]) in [[Biology|biology]]<br/> [[Crystallome|Crystallome]]: The [[Totality|totality]] of&nbsp; ([http://Crystallome.org Crystallome.org])<br/> [[Crystallomics|Crystallomics]]: The [[Omics|omics]] approach research of crystallome ([http://Crystallomics.org Crystallomics.org]) in [[Biology|biology]]</span>
-<span style="font-size: 14px;">[[Constitutionomics|Constitutionomics]]: The omics of all the constitutions in the universe.<br/> [[Contactome|Contactome]]:&nbsp; 2001 The whole set of contacting atoms for all the molecules in cells. Especially proteins that are determined and stor PDB.&nbsp; ([http://Contactome.org Contactome.org])<br/> [[Contactomics|Contactomics]]: The [[Omics|omics]] approach research of Contactome ([http://Contactomics.org Contactomics.org]) in [[Biology|biology]]<br/> [[COVIDomics|COVIDomics]]: [[Covidomics|Covidomics]]: The omics study of coronavirus diseases.<br/> [[Cryptome|Cryptome]]: The [[Totality|totality]] of&nbsp; ([http://Cryptome.org Cryptome.org])<br/> [[Cryptomics|Cryptomics]]: The [[Omics|omics]] approach research of cryptome ([http://Cryptomics.org Cryptomics.org]) in [[Biology|biology]]<br/> [[Crystallome|Crystallome]]: The [[Totality|totality]] of&nbsp; ([http://Crystallome.org Crystallome.org])<br/> [[Crystallomics|Crystallomics]]: The [[Omics|omics]] approach research of crystallome ([http://Crystallomics.org Crystallomics.org]) in [[Biology|biology]]</span>
+<span style="font-size: 14px;">[[CTComics|CTComics]]: The omics study of CTCs (circulating tumor cells)<br/> [[Cyanome|Cyanome]]: The [[Totality|totality]] of&nbsp; ([http://Cyanome.org Cyanome.org])<br/> [[Cyanomics|Cyanomics]]: The [[Omics|omics]] approach research of Cyanome ([http://Cyanomics.org Cyanomics.org]) in [[Biology|biology]]<br/> [[Cybernomics|Cybernomics]]: The omics study of biological systems as recursively feedbacking and intereacting systems in entangled environment ([[Symvironment|Symvironment]])<br/> [[Cytogenomics|Cytogenomics]]: The [[Omics|omics]] approach research on&nbsp;cytogenetics and genomics&nbsp;([http://Cytogenomics.org Cytogenomics.org]) in [[Biology|biology]]<br/> [[Cytokinomics|Cytokinomics]]: The [[Omics|omics]] approach research of cytokinome ([http://Cytokinomics.org Cytokinomics.org]) in [[Biology|biology]]<br/> [[Cytome|Cytome]]: The [[Totality|totality]] of&nbsp; ([http://Cytome.org Cytome.org])<br/> [[Cytomics|Cytomics]]: The [[Omics|omics]] approach research of cytome ([http://Cytomics.org Cytomics.org]) in [[Biology|biology]]<br/> [[Cytosolome|Cytosolome]]: The [[Totality|totality]] of&nbsp; ([http://Cytosolome.org Cytosolome.org])<br/> [[Cytosolomics|Cytosolomics]]: The [[Omics|omics]] approach research of cytosolome ([http://Cytosolomics.org Cytosolomics.org]) in [[Biology|biology]]</span>
 &nbsp;
 === <span style="font-size:20px;">'''--D--'''</span> ===

@@ Line 71: / Line 71: @@
 &nbsp;
 === <span style="font-size:20px;">'''--D--'''</span> ===
@@ Line 80: / Line 81: @@
 <span style="font-size: 14px;">[[Diversomics|Diversomics]]: The omics study of diversity.</span>
-<span style="font-size: 14px;">[[Diversome|Diversome]]: The totality of diversity in genomes, enviromes, and phenomes in the universe.<br/> [[Domainome|Domainome]]: The [[Totality|totality]] of&nbsp; protein domains ([http://Domainome.org Domainome.org])<br/> [[Drugome|Drugome]]: The [[Totality|totality]] of&nbsp;drugs and medicines ([http://Drugome.org Drugome.org]). By BiO center.<br/> [[Drugomics|Drugomics]]: The [[Omics|omics]] approach research of drugome ([http://Drugomics.org Drugomics.org]) in [[Biology|biology]]</span>
+<span style="font-size: 14px;">[[Diversome|Diversome]]: The totality of diversity in genomes, enviromes, and phenomes in the universe.<br/> [[Domainome|Domainome]]: The [[Totality|totality]] of&nbsp; protein domains ([http://Domainome.org Domainome.org])<br/> [[Dosagiomics]]: [[Dosagiome]].&nbsp;<br/> [[Drugome|Drugome]]: The [[Totality|totality]] of&nbsp;drugs and medicines ([http://Drugome.org Drugome.org]). By BiO center.<br/> [[Drugomics|Drugomics]]: The [[Omics|omics]] approach research of drugome ([http://Drugomics.org Drugomics.org]) in [[Biology|biology]]</span>
 &nbsp;

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−	~~<span style~~=~~"font~~-~~size:20px;"><span style="font~~-~~family:Arial~~,~~Helvetica~~,~~sans~~-~~serif;"><span style="color:black"><span style="font~~-~~weight:bold">~~Hormesiomics~~<br/> The~~ omics ~~study~~ of ~~hormesis<~~/~~span><~~/~~span></span></span>~~	+	== Hormesiomics ==
		+
		+	'''Definition'''
		+
		+	Hormesiomics is the systematic, large-scale omics-based investigation of hormetic phenomena in biological systems. It encompasses the comprehensive mapping and analysis of genomic, transcriptomic, proteomic, metabolomic, and epigenomic responses to hormetic stimuli — agents or conditions that elicit adaptive, beneficial effects at low doses and inhibitory or toxic effects at high doses. The field aims to characterize the full molecular architecture of biphasic dose-response landscapes across cell types, tissues, and organisms, with the goal of identifying universal and context-specific hormetic regulators, network topologies, and biological thresholds.
		+
		+	'''Scope'''
		+
		+	Hormesiomics integrates data from multiple omics layers to resolve how organisms sense, transduce, and adapt to sub-threshold stressors — including caloric restriction, exercise-induced oxidative stress, low-dose radiation, xenobiotics, heat shock, and pharmacological senolytics. It applies computational and systems biology approaches to construct hormetic interactomes, identify hormesis-associated biomarkers, and model the dose-response dynamics of adaptive regulatory networks at molecular resolution.
		+
		+	'''Significance'''
		+
		+	As a subfield at the intersection of toxicology, systems biology, and geroscience, hormesiomics provides a quantitative framework for understanding the mechanistic basis of adaptive resilience, stress-response hormones, and longevity-associated pathways. It is particularly relevant to aging research, where hormetic interventions are hypothesized to delay or reverse hallmarks of aging through the activation of conserved stress-response programs such as autophagy, mitophagy, heat shock response, NRF2-mediated antioxidant signaling, and AMPK/mTOR pathway modulation.
		+
		+	'''Coined by'''
		+
		+	Jong Bhak, KOGIC/AgingLab, UNIST, Republic of Korea (2025)
		+
		+	'''See also'''
		+
		+	Hormesis · Geroscience · Geroindex · Omics · Toxicogenomics · Adaptive Stress Response · Senescence · Longevity Biology

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 &nbsp;
 === <span style="font-size:20px;">'''--H--'''</span> ===
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 <span style="font-size: 14px;">[[Hematomics|Hematomics]]: [[Hematome|Hematome]]<br/> [[Herbome|Herbome]]:&nbsp; 2003&nbsp; . The whole set of herbs and their proteins.&nbsp; ([http://Herbome.org Herbome.org])<br/> [[Herbomics|Herbomics]]: The [[Omics|omics]] approach research of Herbome ([http://Herbomics.org Herbomics.org]) in [[Biology|biology]]</span>
-<span style="font-size: 14px;">[[Hologenomics|Hologenomics]]<br/> [[Homome|Homome]]:&nbsp; 2001&nbsp; . The whole of homologous proteins&nbsp; ([http://Homome.org Homome.org])<br/> [[Homomics|Homomics]]: The [[Omics|omics]] approach research of homome ([http://Homomics.org Homomics.org]) in [[Biology|biology]]<br/> [[Hormonome|Hormonome]]:&nbsp; 1999, BiO center. The whole of hormones.&nbsp; ([http://Hormonome.org Hormonome.org])<br/> [[Hormonomics|Hormonomics]]: The [[Omics|omics]] approach research of hormonome ([http://Hormonomics.org Hormonomics.org]) in [[Biology|biology]]<br/> [[Humaninteractome|Humaninteractome]]:&nbsp; 1999 . The whole of human molecular interaction pairs.&nbsp; ([http://Humaninteractome.org Humaninteractome.org])<br/> [[Humaninteractomics|Humaninteractomics]]: The [[Omics|omics]] approach research of humaninteractome ([http://Humaninteractomics.org Humaninteractomics.org]) in [[Biology|biology]]<br/> [[Humanome|Humanome]]:&nbsp; 2004 BiO center. The whole of human beings.&nbsp; ([http://Humanome.org Humanome.org])<br/> [[Humanomics|Humanomics]]:&nbsp; 2004 . The omics study of humans.&nbsp; ([http://Humanomics.org Humanomics.org])<br/> [[Humanpatholome|Humanpatholome]]:&nbsp; 2004 . The pathologies of humans.&nbsp; ([http://Humanpatholome.org Humanpatholome.org])<br/> [[Humanpatholomics|Humanpatholomics]]: The [[Omics|omics]] approach research of humanpatholome ([http://Humanpatholomics.org Humanpatholomics.org]) in [[Biology|biology]]<br/> [[Humanregulome|Humanregulome]]: The [[Totality|totality]] of&nbsp; ([http://Humanregulome.org Humanregulome.org])<br/> [[Humanregulomics|Humanregulomics]]: The [[Omics|omics]] approach research of humanregulome ([http://Humanregulomics.org Humanregulomics.org]) in [[Biology|biology]]<br/> [[Hybridome|Hybridome]]: The [[Totality|totality]] of&nbsp; ([http://Hybridome.org Hybridome.org])<br/> [[Hybridomics|Hybridomics]]: The [[Omics|omics]] approach research of hybridome ([http://Hybridomics.org Hybridomics.org]) in [[Biology|biology]]<br/> [[Hygienome|Hygienome]]: The totality of hygiene related genes and molecules.<br/> [[Hygienomics|Hygienomics]]: The study of hygienes and hygienomes.<br/> [[Hypergenome|Hypergenome]]:</span>
+<span style="font-size: 14px;">[[Hologenomics|Hologenomics]]<br/> [[Homome|Homome]]:&nbsp; 2001&nbsp; . The whole of homologous proteins&nbsp; ([http://Homome.org Homome.org])<br/> [[Homomics|Homomics]]: The [[Omics|omics]] approach research of homome ([http://Homomics.org Homomics.org]) in [[Biology|biology]]<br/> [[Hormonome|Hormonome]]:&nbsp; 1999, BiO center. The whole of hormones.&nbsp; ([http://Hormonome.org Hormonome.org])<br/> [[Hormesiomics|Hormesiomics]]: 2026. BiO Center, Jong Bhak. The omics study of [[Hormesis|hormesis]].<br/> [[Hormonomics|Hormonomics]]: The [[Omics|omics]] approach research of hormonome ([http://Hormonomics.org Hormonomics.org]) in [[Biology|biology]]<br/> [[Humaninteractome|Humaninteractome]]:&nbsp; 1999 . The whole of human molecular interaction pairs.&nbsp; ([http://Humaninteractome.org Humaninteractome.org])<br/> [[Humaninteractomics|Humaninteractomics]]: The [[Omics|omics]] approach research of humaninteractome ([http://Humaninteractomics.org Humaninteractomics.org]) in [[Biology|biology]]<br/> [[Humanome|Humanome]]:&nbsp; 2004 BiO center. The whole of human beings.&nbsp; ([http://Humanome.org Humanome.org])<br/> [[Humanomics|Humanomics]]:&nbsp; 2004 . The omics study of humans.&nbsp; ([http://Humanomics.org Humanomics.org])<br/> [[Humanpatholome|Humanpatholome]]:&nbsp; 2004 . The pathologies of humans.&nbsp; ([http://Humanpatholome.org Humanpatholome.org])<br/> [[Humanpatholomics|Humanpatholomics]]: The [[Omics|omics]] approach research of humanpatholome ([http://Humanpatholomics.org Humanpatholomics.org]) in [[Biology|biology]]<br/> [[Humanregulome|Humanregulome]]: The [[Totality|totality]] of&nbsp; ([http://Humanregulome.org Humanregulome.org])<br/> [[Humanregulomics|Humanregulomics]]: The [[Omics|omics]] approach research of humanregulome ([http://Humanregulomics.org Humanregulomics.org]) in [[Biology|biology]]<br/> [[Hybridome|Hybridome]]: The [[Totality|totality]] of&nbsp; ([http://Hybridome.org Hybridome.org])<br/> [[Hybridomics|Hybridomics]]: The [[Omics|omics]] approach research of hybridome ([http://Hybridomics.org Hybridomics.org]) in [[Biology|biology]]<br/> [[Hygienome|Hygienome]]: The totality of hygiene related genes and molecules.<br/> [[Hygienomics|Hygienomics]]: The study of hygienes and hygienomes.<br/> [[Hypergenome|Hypergenome]]:</span>
 &nbsp;

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−	<span style="font-size:~~37.0pt~~"><span style="font-family:~~" arial="" narrow""="~~"><span style="color:black~~"><span style="language:en-US~~"><span style="font-weight:bold">Hormesiomics<br/> The omics study of hormesis~~</span>~~</span></span></span></span>	+
		+	<span style="font-size:20px;"><span style="font-family:Arial,Helvetica,sans-serif;"><span style="color:black"><span style="font-weight:bold">Hormesiomics<br/> The omics study of hormesis</span></span></span></span>