作者
Jui-Chih Chang, Shou-Jen Kou, Wei-Ting Lin, Chin-San Liu
发表日期
2010/6/6
来源
World journal of cardiology
卷号
2
期号
6
页码范围
150
出版商
Baishideng Publishing Group Inc
简介
Mitochondrial physiology and biogenesis play a crucial role in the initiation and progression of cardiovascular disease following oxidative stress-induced damage such as atherosclerosis (AST). Dysfunctional mitochondria caused by an increase in mitochondrial reactive oxygen species (ROS) production, accumulation of mitochondrial DNA damage, and respiratory chain deficiency induces death of endothelial/smooth muscle cells and favors plaque formation/rupture via the regulation of mitochondrial biogenesis-related genes such as peroxisome proliferator-activated receptor γ coactivator (PGC-1), although more detailed mechanisms still need further study. Based on the effect of healthy mitochondria produced by mitochondrial biogenesis on decreasing ROS-mediated cell death and the recent finding that the regulation of PGC-1 involves mitochondrial fusion-related protein (mitofusin), we thus infer the regulatory …
学术搜索中的文章
JC Chang, SJ Kou, WT Lin, CS Liu - World journal of cardiology, 2010