Cellular senescence and its effector programs.

Cellular senescence and its effector programs.
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DOI:
10.1101/gad.235184.113
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发表时间:
2014-01-15
影响因子:
10.5
通讯作者:
Narita M
Narita M
中科院分区:
生物学1区
文献类型:
--
作者:
Salama R;Sadaie M;Hoare M;Narita M

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细胞衰老可以描述为响应于不同应激的稳定的细胞周期停滞的状态。衰老是多种效应物的集体表型,并且它们的强度和组合可以根据触发物和细胞类型而不同。在这篇综述中,Salama等人总结了效应机制,并强调了衰老集体表型的一些关键组成部分。细胞衰老是伴随细胞周期稳定退出的应激反应。通常,衰老,特别是在人类细胞中,涉及p53和p16/Rb途径,并且通常需要废除这两种肿瘤抑制途径以绕过衰老。与此同时,一些衰老的效应机制已被确定和表征。这些研究表明,衰老是这些多种效应物的集体表型,并且它们的强度和组合可以根据触发物和细胞类型而不同,从而赋予衰老复杂和多样的性质。特别是对衰老相关分泌表型(SASP)的一系列研究揭示了体内衰老细胞的各种功能层。在这里,我们讨论了衰老效应器的一些关键特征,并试图在可能的情况下在功能上将它们联系起来。
Cellular senescence can be described as a state of stable cell cycle arrest in response to diverse stresses. Senescence is a collective phenotype of multiple effectors, and their intensity and combination can be different depending on triggers and cell types. In this review, Salama et al. summarize effector mechanisms and highlight some key components of the collective phenotype of senescence. Cellular senescence is a stress response that accompanies stable exit from the cell cycle. Classically, senescence, particularly in human cells, involves the p53 and p16/Rb pathways, and often both of these tumor suppressor pathways need to be abrogated to bypass senescence. In parallel, a number of effector mechanisms of senescence have been identified and characterized. These studies suggest that senescence is a collective phenotype of these multiple effectors, and their intensity and combination can be different depending on triggers and cell types, conferring a complex and diverse nature to senescence. Series of studies on senescence-associated secretory phenotype (SASP) in particular have revealed various layers of functionality of senescent cells in vivo. Here we discuss some key features of senescence effectors and attempt to functionally link them when it is possible.
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