Cited by 626Mitochondrial Function and PathologyGenetics, Aging, and Longevity in Model OrganismsAutophagy in Disease and Therapy

Mitohormesis

Open access
Yun, Jeanho, Finkel, Toren·2014·Cell Metabolism

Abstract

For many years, mitochondria were viewed as semiautonomous organelles, required only for cellular energetics. This view has been largely supplanted by the concept that mitochondria are fully integrated into the cell and that mitochondrial stresses rapidly activate cytosolic signaling pathways that ultimately alter nuclear gene expression. Remarkably, this coordinated response to mild mitochondrial stress appears to leave the cell less susceptible to subsequent perturbations. This response, termed mitohormesis, is being rapidly dissected in many model organisms. A fuller understanding of mitohormesis promises to provide insight into our susceptibility for disease and potentially provide a unifying hypothesis for why we age.

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Crossref · 10.1016/j.cmet.2014.01.011

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Authors
Yun, J., & Finkel, T.
Affiliations
National Institutes of Health (US)
Corresponding author
Finkel, Toren
Venue
Cell Metabolism
Publisher
Elsevier BV
Published
2014-05
Volume
19
Issue
5
Pages
757-766
ISSN
1550-4131 (ISSN-L)
OpenAlex
W4231604814
Cited by
626
References
91
Citations by year
2026: 38 · 2025: 37 · 2024: 42 · 2023: 51 · 2022: 41 · 2021: 67 · 2020: 64 · 2019: 43 · 2018: 64 · 2017: 56 · 2016: 57 · 2015: 48 · 2014: 18
FWCI
5.62
Type
journal article
Language
en
Open access
Locations
  • Cell Metabolism (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health
  • National Heart, Lung, and Blood Institute (ZIAHL005012)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
Keywords
mitohormesis, mitochondrial stress, mitochondrial signaling, nuclear gene expression, cellular resilience, aging, disease susceptibility
MeSH terms
Animals, Humans, Mitochondria, Stress, Physiological, Signal Transduction, Gene Expression

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