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On the evolution of cellular senescence

期刊

AGING CELL
卷 19, 期 12, 页码 -

出版社

WILEY
DOI: 10.1111/acel.13270

关键词

aging; anti‐ aging; cellular senescence; evolution; senolytics

资金

  1. Federal Ministry of Education and Research (BMBF) of Germany [FKZ 01ZX103A]
  2. US National Institutes of Health [AG069048]
  3. CTSA from the National Center for Advancing Translational Sciences (NCATS) [UL1 TR0002377]
  4. Ted Nash Long Life Foundation
  5. NORDEA Foundation, Denmark [02-2013-0220]
  6. Novo Nordisk Foundation, Denmark [NNF17OC00278]
  7. BBSRC [BB/K017314/1] Funding Source: UKRI

向作者/读者索取更多资源

The idea that senescent cells are causally involved in aging has gained strong support from findings that the removal of such cells alleviates many age-related diseases and extends the life span of mice. While efforts proceed to make therapeutic use of such discoveries, it is important to ask what evolutionary forces might have been behind the emergence of cellular senescence, in order better to understand the biology that we might seek to alter. Cellular senescence is often regarded as an anti-cancer mechanism, since it limits the division potential of cells. However, many studies have shown that senescent cells often also have carcinogenic properties. This is difficult to reconcile with the simple idea of an anti-cancer mechanism. Furthermore, other studies have shown that cellular senescence is involved in wound healing and tissue repair. Here, we bring these findings and ideas together and discuss the possibility that these functions might be the main reason for the evolution of cellular senescence. Furthermore, we discuss the idea that senescent cells might accumulate with age because the immune system had to strike a balance between false negatives (overlooking some senescent cells) and false positives (destroying healthy body cells).

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