Cellular senescence: all roads lead to mitochondria
Open accessAbstract
Senescence is a multi‐functional cell fate, characterized by an irreversible cell‐cycle arrest and a pro‐inflammatory phenotype, commonly known as the senescence‐associated secretory phenotype (SASP). Emerging evidence indicates that accumulation of senescent cells in multiple tissues drives tissue dysfunction and several age‐related conditions. This has spurred the academic community and industry to identify new therapeutic interventions targeting this process. Mitochondrial dysfunction is an often‐unappreciated hallmark of cellular senescence which plays important roles not only in the senescence growth arrest but also in the development of the SASP and resistance to cell‐death. Here, we review the evidence that supports a role for mitochondria in the development of senescence and describe the underlying mechanisms. Finally, we propose that a detailed road map of mitochondrial biology in senescence will be crucial to guide the future development of senotherapies.
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Senescent cell fate can be triggered by many stressors, including DNA damage, oncogene activation, mitochondrial dysfunction, reactive metabolites, oxygen extremes, proteotoxic stress, extracellular signals, infections, mechanical or shear stress, resistance exercise, and factors secreted by other senescent cells.
“The senescent cell fate can be triggered by a number of stressors including DNA damage, cancerous mutations or oncogene activation, mitochondrial dysfunction, reactive metabolites, hyperoxia or hypoxia, proteotoxic stress, extracellular signals, infections, mechanical or shear stresses that deform cells, resistance exercise and factors secreted by other senescent cells18,38–47.”
From Cellular senescence and senolytics: the path to the clinic (2022) · cites this paper as [46]
The Introduction (page not provided) names DNA-damaging agents, oncogene activation, and mitochondrial dysfunction as senescence triggers, and says the senescence-associated secretory phenotype can transmit senescence to healthy cells. The cited paper does not support the full list attributed to it: the passages do not establish oxygen extremes, infections, mechanical or shear stress, or resistance exercise as triggers. (LLM, conf=0.88)
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Cellular senescence and senolytics: the path to the clinic
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The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence
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p21 induces a senescence program and skeletal muscle dysfunction
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Exercise Counters the Age-Related Accumulation of Senescent Cells
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Therapeutic Effects of Mesenchymal Stromal Cells Require Mitochondrial Transfer and Quality Control
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- Authors
- Martini, H., & Passos, J. F.
- Affiliations
- Mayo Clinic (US)
- Corresponding author
- Passos, João F.
- Venue
- The FEBS Journal
- Publisher
- Wiley
- Published
- 2022-01-30
- Volume
- 290
- Issue
- 5
- Pages
- 1186-1202
- ISSN
- 1742-464X (ISSN-L)
- 1742-4658
- PMC
- PMC9296701
- OpenAlex
- W4206639971
- Cited by
- 334
- References
- 155
- Citations by year
- 2026: 74 · 2025: 104 · 2024: 70 · 2023: 67 · 2022: 18 · 2020: 1
- FWCI
- 8.91
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- FEBS Journal (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (1UG3CA 268103‐1)
- National Institute on Aging (1R01AG 68048‐1, P01AG 62413‐1)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- 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
- Keywords
- cellular senescence, mitochondria, mitochondrial dysfunction, senescence-associated secretory phenotype, cell cycle arrest, pro-inflammatory phenotype, senolytics, senotherapy, tissue dysfunction, aging
- MeSH terms
- Mitochondria, Phenotype, Cellular Senescence
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