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How stem cells age and why this makes us grow old

Sharpless, Norman E., DePinho, Ronald A.·2007·Nature Reviews Molecular Cell Biology
DOI 10.1038/nrm2241
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Abstract

Recent data suggest that we age, in part, because our self-renewing stem cells grow old as a result of heritable intrinsic events, such as DNA damage, as well as extrinsic forces, such as changes in their supporting niches. Mechanisms that suppress the development of cancer, such as senescence and apoptosis, which rely on telomere shortening and the activities of p53 and p16(INK4a), may also induce an unwanted consequence: a decline in the replicative function of certain stem-cell types with advancing age. This decreased regenerative capacity appears to contribute to some aspects of mammalian ageing, with new findings pointing to a 'stem-cell hypothesis' for human age-associated conditions such as frailty, atherosclerosis and type 2 diabetes.

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  • Telomere shortening is an important cause of stem cell decline with aging in multiple tissues.

    “Telomere shortening is also an important cause of stem cell decline with aging in multiple tissues”

    From The Hallmarks of Aging (2013) · cites this paper as Sharpless and DePinho, 2007

  • Telomere dysfunction has been causally implicated as a rate-limiting pathogenetic step in age-related diseases including premature aging syndromes, cardiovascular diseases, inflammatory bowel disease, pulmonary fibrosis, metabolic diseases and neurological diseases.

    “Telomere dysfunction has been causally implicated as a rate-limiting pathogenetic step in age-related diseases including premature aging (progeroid) syndromes, cardiovascular diseases, inflammatory bowel disease, pulmonary fibrosis, metabolic diseases and neurological diseases.2,7,8”

    From TERT activation targets DNA methylation and multiple aging hallmarks (2024) · cites this paper as [8]

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Metadata

Authors
Sharpless, N. E., & DePinho, R. A.
Venue
Nature Reviews Molecular Cell Biology
Publisher
Springer Science and Business Media LLC
Published
2007-09
Volume
8
Issue
9
Pages
703-713
ISSN
  • 1471-0072
  • 1471-0080
DOI
10.1038/nrm2241
Cited by
743
References
54
Language
en
Licence
www.springer.com/tdm (tdm)

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