Storer Mekayla, Keyes William M
Centre for Genomic Regulation (CRG); Barcelona, Spain; Universitat Pompeu Fabra (UPF); Barcelona, Spain.
Commun Integr Biol. 2014 Oct 31;7(5). doi: 10.4161/cib.29098. eCollection 2014 Oct.
Cellular senescence is an irreversible form of cell cycle arrest that has been linked to several pathological conditions. In particular, senescence can function as a tumor suppressor mechanism, but is also thought to contribute to organismal aging. Paradoxically however, through the secretion of various factors, collectively termed the senescence-associated secretory phenotype (SASP), senescent cells can also have tumor-promoting and tissue-remodeling functions. In addition, senescent cells can play beneficial roles in tissue repair and wound healing, and reconciling these contradictory features from an evolutionary standpoint has been challenging. Moreover, senescent cells had not previously been documented in non-pathological conditions. Recently however, 2 studies have identified cellular senescence as a programmed mechanism that contributes to tissue patterning and remodeling during normal embryonic development. These findings have significant implications for our understanding of cellular senescence and help to clarify the paradoxes and the evolutionary origin of this process.
细胞衰老一种不可逆的细胞周期停滞形式,与多种病理状况相关。具体而言,衰老可作为一种肿瘤抑制机制发挥作用,但也被认为会促进机体衰老。然而,矛盾的是,通过分泌各种统称为衰老相关分泌表型(SASP)的因子,衰老细胞也可具有促肿瘤和组织重塑功能。此外,衰老细胞在组织修复和伤口愈合中可发挥有益作用,从进化角度协调这些相互矛盾的特征一直具有挑战性。而且,衰老细胞此前未在非病理状况下被记录。然而最近,两项研究已将细胞衰老确定为一种程序性机制,其在正常胚胎发育过程中有助于组织形成和重塑。这些发现对我们理解细胞衰老具有重要意义,并有助于阐明这一过程的矛盾之处及其进化起源。