Mitochondrial dysfunction in cardiovascular disease.
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.
Ballinger
Scott W
SW
Division of Molecular and Cellular Pathology, VH G019F, 1530 3rd Avenue South, Birmingham, AL 35294-0019, USA. sballing@path.uab.edu
D000818:Animals; D002318:Cardiovascular Diseases / Q000209:etiology* / Q000473:pathology*; D006801:Humans; D008929:Mitochondria, Heart / Q000378:metabolism / Q000473:pathology*; D018384:Oxidative Stress; D017382:Reactive Oxygen Species
D017382:Reactive Oxygen Species