Cellular senescence in ageing: from mechanisms to therapeutic opportunities

被引:1337
作者
Di Micco, Raffaella [1 ]
Krizhanovsky, Valery [2 ]
Baker, Darren [3 ,4 ]
di Fagagna, Fabrizio d'Adda [5 ,6 ]
机构
[1] IRCCS San Raffaele Sci Inst, San Raffaele Telethon Inst Gene Therapy SR TIGET, Milan, Italy
[2] Weizmann Inst Sci, Dept Mol Cell Biol, Rehovot, Israel
[3] Mayo Clin, Dept Pediat, Rochester, MN USA
[4] Mayo Clin, Dept Biochem & Mol Biol, Rochester, MN USA
[5] IFOM FIRC Inst Mol Oncol, Milan, Italy
[6] CNR, Ist Genet Mol, Pavia, Italy
基金
欧洲研究理事会; 美国国家卫生研究院; 以色列科学基金会;
关键词
DNA-DAMAGE-RESPONSE; ONCOGENE-INDUCED SENESCENCE; LEUKOCYTE TELOMERE LENGTH; HEMATOPOIETIC STEM-CELLS; SECRETORY PHENOTYPE; DOUBLE-BLIND; LIFE-SPAN; RHEUMATOID-ARTHRITIS; TUMOR SUPPRESSION; MITOCHONDRIAL DYSFUNCTION;
D O I
10.1038/s41580-020-00314-w
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Cellular senescence, first described in vitro in 1961, has become a focus for biotech companies that target it to ameliorate a variety of human conditions. Eminently characterized by a permanent proliferation arrest, cellular senescence occurs in response to endogenous and exogenous stresses, including telomere dysfunction, oncogene activation and persistent DNA damage. Cellular senescence can also be a controlled programme occurring in diverse biological processes, including embryonic development. Senescent cell extrinsic activities, broadly related to the activation of a senescence-associated secretory phenotype, amplify the impact of cell-intrinsic proliferative arrest and contribute to impaired tissue regeneration, chronic age-associated diseases and organismal ageing. This Review discusses the mechanisms and modulators of cellular senescence establishment and induction of a senescence-associated secretory phenotype, and provides an overview of cellular senescence as an emerging opportunity to intervene through senolytic and senomorphic therapies in ageing and ageing-associated diseases.
引用
收藏
页码:75 / 95
页数:21
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