title: Mechanisms of disease: is mitochondrial function altered in heart failure?
abstract: The human heart sustains an exceptional energy transfer rate, consuming more energy per gram weight than any other organ system. The healthy heart can rapidly adapt to changes in demand, while the failing heart cannot. Cardiac energy flux systems falter in the failing heart. The purpose of this review is to characterize the fundamental role of mitochondria in this energy transfer system and describe our local research on mitochondrial respiratory capacity in failing human hearts.
authors.affiliation: Weill Cornell Medical College, New York, New York, USA.
authors.forename: Dale J
authors.initials: DJ
authors.lastname: Hamilton
mesh_terms: D000818:Animals; D017209:Apoptosis; D020013:Calcium Signaling; D019069:Cell Respiration; D004734:Energy Metabolism; D006333:Heart Failure / Q000378:metabolism* / Q000473:pathology / Q000628:therapy; D006801:Humans; D008929:Mitochondria, Heart / Q000378:metabolism* / Q000473:pathology; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D018384:Oxidative Stress
keywords: heart failure; mitochondria; myocardial energetics; oxidative phosphorylation; oximetry; respiratory capacity