title: Apoptotic and non-apoptotic programmed cardiomyocyte death in ventricular remodelling.
abstract: A defining cellular event in the transition from compensated hypertrophy to dilated cardiomyopathy is cardiomyocyte drop-out due to apoptosis, programmed necrosis, and autophagy. The importance of apoptosis in heart failure has been recognized for over a decade, while other forms of programmed cell death have more recently been appreciated, and their pathophysiological roles continue to be defined in experimental and clinical heart failure. The major focus of this review is on apoptosis in heart failure, with a discussion of molecular cross-talk between apoptosis, autophagy, and programmed necrosis.
authors.affiliation: Center for Pharmacogenomics and Cardiovascular Division, Department of Internal Medicine, Washington University, 660 S. Euclid Ave., Campus Box 8086, St Louis, MO 63110, USA. gdorn@dom.wustl.ed
authors.forename: Gerald W
authors.initials: GW
authors.lastname: Dorn
mesh_terms: D000818:Animals; D017209:Apoptosis; D001343:Autophagy; D006332:Cardiomegaly / Q000473:pathology / Q000503:physiopathology; D004721:Endoplasmic Reticulum / Q000378:metabolism; D006333:Heart Failure / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology / Q000628:therapy; D006801:Humans; D008565:Membrane Proteins / Q000378:metabolism; D024101:Mitochondrial Proteins / Q000378:metabolism; D017202:Myocardial Ischemia / Q000473:pathology / Q000503:physiopathology; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000473:pathology*; D009336:Necrosis; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D015398:Signal Transduction; D013312:Stress, Physiological; D020257:Ventricular Remodeling
chemical_list: D008565:Membrane Proteins; D024101:Mitochondrial Proteins; C501741:Nix protein, mouse; D019253:Proto-Oncogene Proteins c-bcl-2
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