Mitochondrial dysfunction in cardiac disease: ischemia--reperfusion, aging, and heart failure.
Mitochondria contribute to cardiac dysfunction and myocyte injury via a loss of metabolic capacity and by the production and release of toxic products. This article discusses aspects of mitochondrial structure and metabolism that are pertinent to the role of mitochondria in cardiac disease. Generalized mechanisms of mitochondrial-derived myocyte injury are also discussed, as are the strengths and weaknesses of experimental models used to study the contribution of mitochondria to cardiac injury. Finally, the involvement of mitochondria in the pathogenesis of specific cardiac disease states (ischemia, reperfusion, aging, ischemic preconditioning, and cardiomyopathy) is addressed.
Lesnefsky
E J
EJ
Division of Cardiology, Case Western Reserve University and Geriatric Research, Education and Clinical Center, Louis Stokes Veterans Affairs Medical Center, Cleveland, Ohio 44106, USA. EXL9@po.cwru.edu
Moghaddas
S
S
Tandler
B
B
Kerner
J
J
Hoppel
C L
CL
D000375:Aging / Q000378:metabolism / Q000502:physiology; D000818:Animals; D002468:Cell Physiological Phenomena; D006331:Heart Diseases / Q000378:metabolism / Q000473:pathology; D006333:Heart Failure / Q000378:metabolism / Q000503:physiopathology*; D006801:Humans; D008928:Mitochondria / Q000378:metabolism / Q000473:pathology / Q000502:physiology*; D017202:Myocardial Ischemia / Q000378:metabolism / Q000503:physiopathology*; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000503:physiopathology*; D009206:Myocardium / Q000166:cytology / Q000378:metabolism