Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (599 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Biphasic dose responses of cells or organisms (including microorganisms) to an exogenous or intrinsic factor, in which the factor induces stimulatory or beneficial effects at low doses and inhibitory or adverse effects at high doses.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Hormeses; Hormetic Dose-Response; Dose-Response, Hormetic; Dose-Responses, Hormetic; Hormetic Dose Response; Hormetic Dose-Responses.
Where it fits in the MeSH classification
- Broader topics
- Dose-Response Relationship, Drug
Research landscape
PubMed indexes 962 records tagged with the MeSH heading “Hormesis” (counts retrieved 2026-10-29). 475 of them (49.4%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 497 records.
Reviews account for 296 records (30.8%) and meta-analyses for 6. Randomized controlled trials number 2 (0.2%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 0 |
| 2000-2009 | 1 |
| 2010-2019 | 497 |
| 2020 onward | 475 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 296 | 30.8% |
| Meta-analyses | 6 | 0.6% |
| Randomized controlled trials | 2 | 0.2% |
Method: PubMed query "Hormesis"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in pharmacology
Drug evidence builds in layers: laboratory pharmacology describes how a compound acts, pharmacokinetic studies describe how the body handles it, and randomized trials test whether it helps and what harms it causes. Post-marketing surveillance and observational studies reveal rarer adverse effects but cannot prove causation. This page is educational and is not a recommendation to start, stop or change any medicine; decisions about treatment belong with a qualified clinician.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Hormetic heat stress and HSF-1 induce autophagy to improve survival and proteostasis in C. elegans | 2017 | Research article Design not recorded in structured metadata | 251 | cc by PMID 28198373 · DOI · PMC5316864 |
| Lithium Promotes Longevity through GSK3/NRF2-Dependent Hormesis | 2016 | Research article Design not recorded in structured metadata | 160 | cc by PMID 27068460 · DOI · PMC4850359 |
| Hormesis: Path and Progression to Significance | 2018 | Review article Design not recorded in structured metadata | 158 | cc by PMID 30248927 · DOI · PMC6213774 |
| Moderate nutritional stress reprogrammes insulin responses to drive enhanced starvation tolerance in Drosophila melanogaster | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 41378461 · DOI · PMC12891944 |
Hormetic heat stress and HSF-1 induce autophagy to improve survival and proteostasis in C. elegans [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Stress-response pathways have evolved to maintain cellular homeostasis and to ensure the survival of organisms under changing environmental conditions.
- Closing excerpt
- These findings demonstrate that autophagy contributes to stress resistance and hormesis, and reveal a requirement for autophagy in HSF-1-regulated functions in the heat-shock response, proteostasis and ageing.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (150 words)
Stress-response pathways have evolved to maintain cellular homeostasis and to ensure the survival of organisms under changing environmental conditions. Whereas severe stress is detrimental, mild stress can be beneficial for health and survival, known as hormesis. Although the universally conserved heat-shock response regulated by transcription factor HSF-1 has been implicated as an effector mechanism, the role and possible interplay with other cellular processes, such as autophagy, remains poorly understood. Here we show that autophagy is induced in multiple tissues of Caenorhabditis elegans following hormetic heat stress or HSF-1 overexpression. Autophagy-related genes are required for the thermoresistance and longevity of animals exposed to hormetic heat shock or HSF-1 overexpression. Hormetic heat shock also reduces the progressive accumulation of PolyQ aggregates in an autophagy-dependent manner. These findings demonstrate that autophagy contributes to stress resistance and hormesis, and reveal a requirement for autophagy in HSF-1-regulated functions in the heat-shock response, proteostasis and ageing.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 28198373 · DOI · PMC5316864
Lithium Promotes Longevity through GSK3/NRF2-Dependent Hormesis [2]
Abstract reading summary — source excerpts
- Opening excerpt
- The quest to extend healthspan via pharmacological means is becoming increasingly urgent, both from a health and economic perspective.
- Closing excerpt
- The discovery of GSK-3 as a therapeutic target for aging will likely lead to more effective treatments that can modulate mammalian aging and further improve health in later life.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (137 words)
The quest to extend healthspan via pharmacological means is becoming increasingly urgent, both from a health and economic perspective. Here we show that lithium, a drug approved for human use, promotes longevity and healthspan. We demonstrate that lithium extends lifespan in female and male Drosophila, when administered throughout adulthood or only later in life. The life-extending mechanism involves the inhibition of glycogen synthase kinase-3 (GSK-3) and activation of the transcription factor nuclear factor erythroid 2-related factor (NRF-2). Combining genetic loss of the NRF-2 repressor Kelch-like ECH-associated protein 1 (Keap1) with lithium treatment revealed that high levels of NRF-2 activation conferred stress resistance, while low levels additionally promoted longevity. The discovery of GSK-3 as a therapeutic target for aging will likely lead to more effective treatments that can modulate mammalian aging and further improve health in later life.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 27068460 · DOI · PMC4850359
Hormesis: Path and Progression to Significance [3]
Abstract reading summary — source excerpts
- Opening excerpt
- This paper tells the story of how hormesis became recognized as a fundamental concept in biology, affecting toxicology, microbiology, medicine, public health, agriculture, and all areas related to enhancing biological performance.
- Closing excerpt
- This paper also explains the application of hormesis to several neurodegenerative diseases such as Parkinson's and Huntington's disease, macrophage polarization and its systematic adaptive protections, and the role of hormesis in enhancing stem cell functioning and medical applications.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (102 words)
This paper tells the story of how hormesis became recognized as a fundamental concept in biology, affecting toxicology, microbiology, medicine, public health, agriculture, and all areas related to enhancing biological performance. This paper assesses how hormesis enhances resilience to normal aging and protects against a broad spectrum of neurodegenerative, cardiovascular, and other diseases, as well as trauma and other threats to health and well-being. This paper also explains the application of hormesis to several neurodegenerative diseases such as Parkinson's and Huntington's disease, macrophage polarization and its systematic adaptive protections, and the role of hormesis in enhancing stem cell functioning and medical applications.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 30248927 · DOI · PMC6213774
Moderate nutritional stress reprogrammes insulin responses to drive enhanced starvation tolerance in Drosophila melanogaster [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Organisms in the wild constantly encounter fluctuations in temperature and food availability, pathogens and other stressors that disrupt their physiological balance.
- Closing excerpt
- These insights will improve our understanding of the molecular and metabolic mechanisms driving hormesis, with broader implications for stress resilience and organismal health.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (210 words)
Organisms in the wild constantly encounter fluctuations in temperature and food availability, pathogens and other stressors that disrupt their physiological balance. To counteract these disruptions, organisms initiate stress responses that vary in nature depending on the intensity and duration of the stressor. While severe stress can be harmful or even fatal, moderate stress can activate adaptive mechanisms, a phenomenon known as hormesis. Hormesis enhances resilience to stress and has been associated with improved ageing, immunity and metabolism. Short-term exposures to mild stress, such as heat or oxidative stress, have been shown to extend Drosophila lifespan and promote cross-tolerance to other stressors. Among various environmental stressors, starvation poses a significant and recurring challenge that has driven the evolution of energy-conserving strategies essential for survival. Prior exposure to starvation has been shown to influence longevity, resilience to starvation, physiological status and stress tolerance. However, the mechanisms underlying these hormetic effects remain poorly understood. In this study, we investigated how short-term starvation enhances resistance to prolonged food deprivation in Drosophila. Our findings reveal that metabolic rewiring, including changes in energy utilization, insulin signalling and transcriptomic profiles, underpins this adaptive plasticity. These insights will improve our understanding of the molecular and metabolic mechanisms driving hormesis, with broader implications for stress resilience and organismal health.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41378461 · DOI · PMC12891944
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Hormetic mechanisms [5]
- Research article Cellular stress responses, hormetic phytochemicals and vitagenes in aging and longevity [6]
- Research article Insecticide-induced hormesis and arthropod pest management [7]
- Research article Preconditioning is hormesis part I: Documentation, dose-response features and mechanistic foundations [8]
- Research article Hormesis, cellular stress response and vitagenes as critical determinants in aging and longevity [9]
- Research article Preconditioning is hormesis part II: How the conditioning dose mediates protection: Dose optimization within temporal and mechanistic frameworks [10]
References
- Kumsta C, Chang JT, Schmalz J, Hansen M. Hormetic heat stress and HSF-1 induce autophagy to improve survival and proteostasis in C. elegans. . 2017. PMID 28198373 · DOI · PMC5316864
- Castillo-Quan JI, Li L, Kinghorn KJ, Ivanov DK, Tain LS, Slack C, et al.. Lithium Promotes Longevity through GSK3/NRF2-Dependent Hormesis. . 2016. PMID 27068460 · DOI · PMC4850359
- Calabrese EJ. Hormesis: Path and Progression to Significance. . 2018. PMID 30248927 · DOI · PMC6213774
- Menon RV, Varghese J. Moderate nutritional stress reprogrammes insulin responses to drive enhanced starvation tolerance in Drosophila melanogaster. . 2026. PMID 41378461 · DOI · PMC12891944
- Calabrese EJ. Hormetic mechanisms. Crit Rev Toxicol. 2013. PMID 23875765 · DOI
- Calabrese V, Cornelius C, Dinkova-Kostova AT, Iavicoli I, Di Paola R, Koverech A, et al.. Cellular stress responses, hormetic phytochemicals and vitagenes in aging and longevity. Biochim Biophys Acta. 2012. PMID 22108204 · DOI
- Guedes RN, Cutler GC. Insecticide-induced hormesis and arthropod pest management. Pest Manag Sci. 2014. PMID 24155227 · DOI
- Calabrese EJ. Preconditioning is hormesis part I: Documentation, dose-response features and mechanistic foundations. Pharmacol Res. 2016. PMID 26757428 · DOI
- Calabrese V, Cornelius C, Cuzzocrea S, Iavicoli I, Rizzarelli E, Calabrese EJ. Hormesis, cellular stress response and vitagenes as critical determinants in aging and longevity. Mol Aspects Med. 2011. PMID 22020114 · DOI
- Calabrese EJ. Preconditioning is hormesis part II: How the conditioning dose mediates protection: Dose optimization within temporal and mechanistic frameworks. Pharmacol Res. 2016. PMID 26748033 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.