发病机制
杂合子丢失
疾病
体细胞
DNA损伤
生物
基因组不稳定性
致癌物
突变
癌症研究
遗传学
病理
生物信息学
免疫学
医学
基因
DNA
等位基因
作者
Maria Grazia Andreassi,Nicoletta Botto
标识
DOI:10.1016/s1050-1738(03)00109-9
摘要
Atherosclerosis is the leading cause of illness and death in Western societies. It is now clear that the disease is a result of a chronic fibroproliferative-inflammatory response of the arterial intima leading to the formation of atherosclerotic plaque. There is, however, strong experimental evidence for a "mutation theory of atherosclerosis," underlining the similarity between atherosclerotic and carcinogenic processes. This review provides an overview of the studies that support the role of genetic alterations in the disease. The demonstration of microsatellite instability and loss of heterozygosity in smooth muscle cells of human plaques suggests that genomic destabilization may play a pivotal role in atherosclerotic mechanisms. Furthermore, the use of accepted biomarkers of carcinogenic exposure-such as DNA adducts and cytogenetic end points-recently has provided evidence consistent with the view that somatic cell alterations are critical in atherogenic process. It follows that the study of DNA damage may provide new insights into the pathogenesis of atherosclerosis and lead to the development of novel therapeutic approaches.
科研通智能强力驱动
Strongly Powered by AbleSci AI