DNA Damage and Repair in Vascular Disease

被引:64
作者
Uryga, Anna [1 ]
Gray, Kelly [2 ]
Bennett, Martin [1 ]
机构
[1] Univ Cambridge, Div Cardiovasc Med, Cambridge CB2 0QQ, England
[2] AstraZeneca, Cardiovasc Safety, Cambridge CB4 0FZ, England
来源
ANNUAL REVIEW OF PHYSIOLOGY, VOL 78 | 2016年 / 78卷
基金
英国医学研究理事会;
关键词
senescence; DNA damage; atherosclerosis; DNA repair; STRAND-BREAK REPAIR; SMOOTH-MUSCLE-CELLS; BASE-EXCISION-REPAIR; TELOMERE LENGTH; CHECKPOINT CONTROL; ATHEROSCLEROTIC LESIONS; CARDIOVASCULAR-DISEASE; MAMMALIAN TELOMERES; CYCLE CHECKPOINTS; SENESCENT CELLS;
D O I
10.1146/annurev-physiol-021115-105127
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
DNA damage affecting both genomic and mitochondrial DNA is present in a variety of both inherited and acquired vascular diseases. Multiple cell types show persistent DNA damage and a range of lesions. In turn, DNA damage activates a variety of DNA repair mechanisms, many of which are activated in vascular disease. Such DNA repair mechanisms either stall the cell cycle to allow repair to occur or trigger apoptosis or cell senescence to prevent propagation of damaged DNA. Recent evidence has indicated that DNA damage occurs early, is progressive, and is sufficient to impair function of cells composing the vascular wall. The consequences of persistent genomic and mitochondrial DNA damage, including inflammation, cell senescence, and apoptosis, are present in vascular disease. DNA damage can thus directly cause vascular disease, opening up new possibilities for both prevention and treatment. We review the evidence for and the causes, types, and consequences of DNA damage in vascular disease.
引用
收藏
页码:45 / 66
页数:22
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