Mitochondrial energy metabolism in heart failure: a question of balance.
The mitochondrion serves a critical role as a platform for energy transduction, signaling, and cell death pathways relevant to common diseases of the myocardium such as heart failure. This review focuses on the molecular regulatory events and downstream effector pathways involved in mitochondrial energy metabolic derangements known to occur during the development of heart failure.
Huss
Janice M
JM
Center for Cardiovascular Research, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
Kelly
Daniel P
DP
D000818:Animals; D002303:Cardiac Output, Low / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D006332:Cardiomegaly / Q000378:metabolism / Q000503:physiopathology; D019069:Cell Respiration / Q000502:physiology; D004734:Energy Metabolism; D006360:Heat-Shock Proteins / Q000235:genetics / Q000378:metabolism; D006801:Humans; D008928:Mitochondria / Q000378:metabolism*; D009206:Myocardium / Q000166:cytology / Q000378:metabolism* / Q000473:pathology; D000071248:Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; D015398:Signal Transduction / Q000502:physiology; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism; D014158:Transcription, Genetic
D006360:Heat-Shock Proteins; C486497:PPARGC1A protein, human; D000071248:Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; D014157:Transcription Factors