Cellular lifespan and senescence signaling in embryonic stem cells
Open accessAbstract
Summary: Most mammalian cells when placed in culture will undergo a limited number of cell divisions before entering an unresponsive non‐proliferating state termed senescence. However, several pathways that are activated singly or in concert can allow cells to bypass senescence at least for limited periods. These include the telomerase pathway required to maintain telomere ends, the p53 and Rb pathways required to direct senescence in response to DNA damage, telomere shortening and mitogenic signals, and the insulin‐like growth factor – Akt pathway that may regulate lifespan and cell proliferation. In this review, we summarize recent findings related to these pathways in embryonic stem (ES) cells and suggest that ES cells are immortal because these pathways are tightly regulated.
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Embryonic stem cells, whether human or rodent, express high levels of telomerase and thus do not undergo replicative senescence in culture or in vivo.
“Embryonic stem cells, whether human or rodent, express high levels of telomerase and thus do not undergo replicative senescence in culture or in vivo (Odorico et al., 2001; Miura et al., 2004).”
From Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors (2005) · cites this paper as Miura et al., 2004
The Introduction says ES cells appear able to bypass senescence, and “Role of telomerase in ES cell self-renewal” reports high telomerase activity in human and mouse ES cells, including during prolonged culture. The paper does not establish that ES cells avoid replicative senescence in vivo, and it presents telomerase as one of several pathways involved rather than the sole demonstrated cause. Page numbers were not available in our copy. (LLM, conf=0.87)
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- Authors
- Miura, T., Mattson, M. P., & Rao, M. S.
- Affiliations
- National Institute on Aging (US)
- Johns Hopkins University (US)
- Corresponding author
- Rao, Mahendra S.
- ORCID
- Mattson, Mark P.
- Venue
- Aging Cell
- Publisher
- Wiley
- Published
- 2004-11
- Volume
- 3
- Issue
- 6
- Pages
- 333-343
- ISSN
- 1474-9718 (ISSN-L)
- 1474-9726
- OpenAlex
- W1591789003
- Cited by
- 102
- References
- 130
- Citations by year
- 2024: 2 · 2023: 2 · 2022: 2 · 2021: 4 · 2020: 3 · 2018: 9 · 2017: 4 · 2016: 3 · 2014: 7 · 2013: 10 · 2012: 7
- FWCI
- 0.89
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Aging Cell (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging
- 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 › Pluripotent Stem Cells Research
- Keywords
- cellular senescence, embryonic stem cells, cellular lifespan, telomerase, telomere shortening, p53 pathway, Rb pathway, DNA damage response, insulin-like growth factor, Akt signaling, cell proliferation, cell immortalization
- MeSH terms
- Embryo, Mammalian, Humans, Models, Biological, Stem Cells, Signal Transduction, Cellular Senescence
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