Rapamycin decelerates cellular senescence
Open accessAbstract
When the cell cycle is arrested but cellular growth is not, then cells senesce, permanently losing proliferative potential. Here we demonstrated that the duration of cell cycle arrest determines a progressive loss of proliferative capacity. In human and rodent cell lines, rapamycin (an inhibitor of mTOR) dramatically decelerated loss of proliferative potential caused by ectopic p21, p16 and sodium butyrate-induced p21. Thus, when the cell cycle was arrested by these factors in the presence of rapamycin, cells retained the capacity to resume proliferation, once p21, p16 or sodium butyrate were removed. While rapamycin prevented the permanent loss of proliferative potential in arrested cells, it did not force the arrested cells into proliferation. During cell cycle arrest, rapamycin transformed the irreversible arrest into a reversible condition. Our data demonstrate that senescence can be pharmacologically suppressed.
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mTOR positively regulates senescence in different systems.
“Interestingly, a number of studies have shown that mTOR, a master regulator of protein synthesis, also positively regulates senescence in different systems (Demidenko et al. 2009; Blagosklonny 2012; Kolesnichenko et al. 2012; Pospelova et al. 2012; Garbers et al. 2013).”
From Cellular senescence and its effector programs (2014) · cites this paper as Demidenko et al. 2009
Rapamycin inhibits cell senescence in vitro.
“Rapamycin, an inhibitor of mTOR, inhibits cell senescence in vitro and increases longevity in several species.”
From Rapamycin inhibits the secretory phenotype of senescent cells by a Nrf2-independent mechanism (2017) · cites this paper as Demidenko et al., 2009
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References 16 · Cited by 391
- Authors
- Demidenko, Z. N., Zubova, S. G., Bukreeva, E. I., Pospelov, V. A., Pospelova, T. V., & Blagosklonny, M. V.
- Affiliations
- Institute of Cytology (RU)
- Corresponding author
- Blagosklonny, Mikhail V
- ORCID
- Zubova, Svetlana G.
- Venue
- Cell Cycle
- Publisher
- Informa UK Limited
- Published
- 2009-06-15
- Volume
- 8
- Issue
- 12
- Pages
- 1888-1895
- ISSN
- 1538-4101 (ISSN-L)
- 1551-4005
- OpenAlex
- W1982695619
- Cited by
- 391
- References
- 16
- Citations by year
- 2026: 8 · 2025: 7 · 2024: 12 · 2023: 6 · 2022: 21 · 2021: 11 · 2020: 20 · 2019: 22 · 2018: 19 · 2017: 20 · 2016: 23 · 2015: 23 · 2014: 38 · 2013: 32 · 2012: 46
- FWCI
- 28.22
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cell Cycle (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Russian Foundation for Basic Research
- National Institutes of Health (1r41ey018520-01)
- Russian Academy of Sciences
- National Eye Institute (1 R41 EY018520-01)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Keywords
- cellular senescence, rapamycin, mTOR inhibition, cell cycle arrest, proliferative capacity, p21, p16, sodium butyrate
- MeSH terms
- Animals, Butyrates, Cell Cycle, Cell Line, Humans, Isopropyl Thiogalactoside, Neoplasm Proteins, Protein Kinases, Cellular Senescence, Cyclin-Dependent Kinase Inhibitor p16, Sirolimus, Cell Line, Tumor, Cyclin-Dependent Kinase Inhibitor p21, Mice, TOR Serine-Threonine Kinases
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