Aging, Cellular Senescence, and Cancer

被引:1879
|
作者
Campisi, Judith [1 ,2 ]
机构
[1] Buck Inst Res Aging, Novato, CA 94945 USA
[2] Univ Calif Berkeley, Lawrence Berkeley Natl Lab, Berkeley, CA 94720 USA
来源
关键词
antagonistic pleiotropy; DNA damage; inflammation; stress response; tumor suppression; DNA-DAMAGE-RESPONSE; ONCOGENE-INDUCED SENESCENCE; PREMATURE SENESCENCE; SECRETORY PHENOTYPE; IN-VIVO; REPLICATIVE SENESCENCE; HUMAN-CELLS; FIBROBLAST SENESCENCE; STROMAL FIBROBLASTS; STELLATE CELLS;
D O I
10.1146/annurev-physiol-030212-183653
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
For most species, aging promotes a host of degenerative pathologies that are characterized by debilitating losses of tissue or cellular function. However, especially among vertebrates, aging also promotes hyperplastic pathologies, the most deadly of which is cancer. In contrast to the loss of function that characterizes degenerating cells and tissues, malignant (cancerous) cells must acquire new (albeit aberrant) functions that allow them to develop into a lethal tumor. This review discusses the idea that, despite seemingly opposite characteristics, the degenerative and hyperplastic pathologies of aging are at least partly linked by a common biological phenomenon: a cellular stress response known as cellular senescence. The senescence response is widely recognized as a potent tumor suppressive mechanism. However, recent evidence strengthens the idea that it also drives both degenerative and hyperplastic pathologies, most likely by promoting chronic inflammation. Thus, the senescence response may be the result of antagonistically pleiotropic gene action.
引用
收藏
页码:685 / 705
页数:21
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