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衰老停滞程序与细胞周期。

The senescence arrest program and the cell cycle.

作者信息

Bitto Alessandro, Crowe Elizabeth P, Lerner Chad, Torres Claudio, Sell Christian

机构信息

Department of Pathology, University of Washington, Health Science Building D-514, Seattle, 357470, WA, USA.

出版信息

Methods Mol Biol. 2014;1170:145-54. doi: 10.1007/978-1-4939-0888-2_8.

Abstract

All living organisms are subject to progressive loss of function and damage to their tissues, a process known as aging. At the cellular level, the accumulation of damage to DNA, proteins, and organelles induces cellular senescence, a stress-response pathway that likely influences the aging process. Although the senescence arrest program was initially described in vitro, accumulating evidence suggests that this damage response program occurs in a variety of pathologic settings. This review discusses aspects of the senescence program, their interrelationships with damage arrest pathways, the cell cycle, and the impact of senescence in vivo.

摘要

所有生物都会经历功能的逐渐丧失以及组织损伤,这一过程被称为衰老。在细胞层面,DNA、蛋白质和细胞器的损伤积累会引发细胞衰老,这是一种可能影响衰老过程的应激反应途径。尽管衰老停滞程序最初是在体外被描述的,但越来越多的证据表明,这种损伤反应程序发生在多种病理环境中。本综述讨论了衰老程序的各个方面、它们与损伤停滞途径、细胞周期的相互关系以及衰老在体内的影响。

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