Mitochondrial dysfunction in cardiovascular disease

被引:319
作者
Ballinger, SW [1 ]
机构
[1] Div Mol & Cellular Pathol, Birmingham, AL 35294 USA
关键词
mitochondria; cardiovascular; atherosclerosis; mtDNA; oxidative stress;
D O I
10.1016/j.freeradbiomed.2005.02.014
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Whereas the pathogenesis of atherosclerosis has been intensively studied and described, the underlying events that initiate cardiovascular disease are not yet fully understood. A substantial number of studies suggest that altered levels of oxidative and nitrosoxidative stress within the cardiovascular environment are essential in the development of cardiovascular disease; however, the impact of such changes on the subcellular or organellar components and their functions that are relevant to cardiovascular disease inception are less understood. In this regard, studies are beginning to show that mitochondria not only appear susceptible to damage mediated by increased oxidative and nitrosoxidative stress, but also play significant roles in the regulation of cardiovascular cell function. In addition, accumulating evidence suggests that a common theme among cardiovascular disease development and cardiovascular disease risk factors is increased mitochondrial damage and dysfunction. This review discusses aspects relating mitochondrial damage and function to cardiovascular disease risk factors and disease development. (c) 2005 Elsevier Inc. All rights reserved.
引用
收藏
页码:1278 / 1295
页数:18
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