衰老
端粒
DNA损伤
细胞老化
生物
表观遗传学
活性氧
细胞衰老
细胞生物学
免疫学
表型
遗传学
DNA
基因
作者
Julie C. Wang,Martin R. Bennett
出处
期刊:Circulation Research
[Ovid Technologies (Wolters Kluwer)]
日期:2012-07-06
卷期号:111 (2): 245-259
被引量:659
标识
DOI:10.1161/circresaha.111.261388
摘要
Atherosclerosis is classed as a disease of aging, such that increasing age is an independent risk factor for the development of atherosclerosis. Atherosclerosis is also associated with premature biological aging, as atherosclerotic plaques show evidence of cellular senescence characterized by reduced cell proliferation, irreversible growth arrest and apoptosis, elevated DNA damage, epigenetic modifications, and telomere shortening and dysfunction. Not only is cellular senescence associated with atherosclerosis, there is growing evidence that cellular senescence promotes atherosclerosis. This review examines the pathology of normal vascular aging, the evidence for cellular senescence in atherosclerosis, the mechanisms underlying cellular senescence including reactive oxygen species, replication exhaustion and DNA damage, the functional consequences of vascular cell senescence, and the possibility that preventing accelerated cellular senescence is a therapeutic target in atherosclerosis.
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