Healing and Hurting: Molecular Mechanisms, Functions, and Pathologies of Cellular Senescence

被引:252
作者
Adams, Peter D. [1 ]
机构
[1] Univ Glasgow, Canc Res UK Beatson Labs, Glasgow G61 1BD, Lanark, Scotland
基金
美国国家卫生研究院;
关键词
ONCOGENE-INDUCED SENESCENCE; DEMETHYLASE JMJD3 CONTRIBUTES; GENOME-WIDE ASSOCIATION; HUMAN ENDOTHELIAL-CELLS; DNA-DAMAGE; LIFE-SPAN; P38; MAPK; IN-VITRO; MATRIX METALLOPROTEINASES; REPLICATIVE SENESCENCE;
D O I
10.1016/j.molcel.2009.09.021
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Cellular senescence is a proliferation arrest that is typically irreversible and caused by various cellular stresses, including excess rounds of cell division and cancer-causing genetic alterations. Senescence actively contributes to a tissue-level response to tissue wounding and incipient cancer, healing the tissue and suppressing tumor formation. However, in the long term, the same senescence program may hurt the tissue, thereby contributing to tissue aging. Tumor suppression, wound healing, and aging are each associated with inflammation, and here it is proposed that cellular senescence contributes to a "nonimmune cell" component of the tissue inflammatory response.
引用
收藏
页码:2 / 14
页数:13
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