Autophagy and senescence: A partnership in search of definition
Open accessAbstract
Autophagy and senescence share a number of characteristics, which suggests that both responses could serve to collaterally protect the cell from the toxicity of external stress such as radiation and chemotherapy and internal forms of stress such as telomere shortening and oncogene activation. Studies of oncogene activation in normal fibroblasts as well as exposure of tumor cells to chemotherapy have indicated that autophagy and senescence are closely related but not necessarily interdependent responses; specifically, interference with autophagy delays but does not abrogate senescence. The literature relating to this topic is inconclusive, with some reports appearing to be consistent with a direct relationship between autophagy and senescence and others indicative of an inverse relationship. Before this question can be resolved, additional studies will be necessary where autophagy is clearly inhibited by genetic silencing and where the temporal responses of both autophagy and senescence are monitored, preferably in cells that are intrinsically incapable of apoptosis or where apoptosis is suppressed. Understanding the nature of this relationship may provide needed insights relating to cytoprotective as well as potential cytotoxic functions of both autophagy and senescence.
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Other findings indicate that inhibiting autophagy promotes senescence in some contexts.
“other findings indicate that autophagy inhibition promotes senescence in some contexts (33).”
From The DNA damage response induces inflammation and senescence by inhibiting autophagy of GATA4. (2015) · cites this paper as [33]
Autophagy is both a negative and a positive regulator of senescence, resolving apparently contradictory reports in the literature.
“Our results indicate that autophagy is both a negative and a positive regulator of senescence, resolving apparently contradictory reports in the literature (31–33, 44).”
From The DNA damage response induces inflammation and senescence by inhibiting autophagy of GATA4. (2015) · cites this paper as [33]
Autophagy is activated during senescence.
“Autophagy is activated during senescence”
From Inside and out: the activities of senescence in cancer (2014) · cites this paper as [73]
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- Authors
- Gewirtz, D. A.
- Affiliations
- Virginia Commonwealth University (US)
- Corresponding author
- Gewirtz, David A.
- ORCID
- Gewirtz, David A.
- Venue
- Autophagy
- Publisher
- Informa UK Limited
- Published
- 2013-05-06
- Volume
- 9
- Issue
- 5
- Pages
- 808-812
- ISSN
- 1554-8627 (ISSN-L)
- 1554-8635
- PMC
- PMC3669198
- OpenAlex
- W2021163182
- Cited by
- 166
- References
- 32
- Citations by year
- 2026: 3 · 2025: 5 · 2024: 10 · 2023: 12 · 2022: 17 · 2021: 23 · 2020: 15 · 2019: 14 · 2018: 18 · 2017: 14 · 2016: 16 · 2015: 11 · 2014: 7 · 2013: 1
- FWCI
- 8.50
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Autophagy (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- cellular senescence, oncogene activation, telomere shortening, chemoresistance, radioresistance (biology), cytoprotection, apoptosis, cancer cells, fibroblasts, stress response
- MeSH terms
- Animals, Autophagy, Fibroblasts, Humans, Neoplasms, Signal Transduction, Cellular Senescence, Apoptosis, Reactive Oxygen Species, Cytoprotection, Endothelial Cells, Cell Line, Tumor, Mice
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