Senescent cells, tumor suppression, and organismal aging: Good citizens, bad neighbors

被引：1821

作者：

Campisi, J ^{[1
]}

机构：

[1] Lawrence Berkeley Lab, Berkeley, CA 94720 USA

[2] Buck Inst Age Res, Novato, CA 94545 USA

来源：

CELL | 2005年 / 120卷 / 04期

基金：

美国国家卫生研究院;

关键词：

D O I：

10.1016/j.cell.2005.02.003

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：

Cells from organisms with renewable tissues can permanently withdraw from the cell cycle in response to diverse stress, including dysfunctional telomeres, DNA damage, strong mitogenic signals, and disrupted chromatin. This response, termed cellular senescence, is controlled by the p53 and RB tumor suppressor proteins and constitutes a potent anticancer mechanism. Nonetheless, senescent cells acquire phenotypic changes that may contribute to aging and certain age-related diseases, including late-life cancer. Thus, the senescence response may be antagonistically pleiotropic, promoting early-life survival by curtailing the development of cancer but eventually limiting longevity as dysfunctional senescent cells accumulate.

引用

页码：513 / 522

页数：10

共 101 条

[1] Involvement of the cyclin-dependent kinase inhibitor p16 (INK4a) in replicative senescence of normal human fibroblasts [J].