Cellular senescence: from physiology to pathology

被引:2328
作者
Munoz-Espin, Daniel [1 ]
Serrano, Manuel [1 ]
机构
[1] Spanish Natl Canc Res Ctr CNIO, Tumour Suppress Grp, E-28029 Madrid, Spain
基金
欧洲研究理事会;
关键词
DNA-DAMAGE-RESPONSE; ONCOGENE-INDUCED SENESCENCE; GENOME-WIDE ASSOCIATION; TUMOR-SUPPRESSOR; CHONDROCYTE SENESCENCE; PULMONARY-HYPERTENSION; ACCELERATED SENESCENCE; SECRETORY PHENOTYPE; OXIDATIVE STRESS; KNOCKOUT MICE;
D O I
10.1038/nrm3823
中图分类号
Q2 [细胞生物学];
学科分类号
071013 [干细胞生物学];
摘要
Recent discoveries are redefining our view of cellular senescence as a trigger of tissue remodelling that acts during normal embryonic development and upon tissue damage. To achieve this, senescent cells arrest their own proliferation, recruit phagocytic immune cells and promote tissue renewal. This sequence of events-senescence, followed by clearance and then regeneration-may not be efficiently completed in aged tissues or in pathological contexts, thereby resulting in the accumulation of senescent cells. Increasing evidence indicates that both pro-senescent therapies and antisenescent therapies can be beneficial. In cancer and during active tissue repair, pro-senescent therapies contribute to minimize the damage by limiting proliferation and fibrosis, respectively. Conversely, antisenescent therapies may help to eliminate accumulated senescent cells and to recover tissue function.
引用
收藏
页码:482 / +
页数:15
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