title: Mechanisms of apoptosis in the heart.
abstract: Apoptosis is a complex and highly regulated form of cell death, and believed to contribute to the continuous decline of ventricular function in heart failure. Apoptotic cell death is observed in a variety of cardiovascular diseases, including myocardial infarction, ischemia-reperfusion injury, end-stage heart failure, arrhythmias, and adriamycin cardiomyopathy. There are several pathways leading to programmed cell death. Apoptosis can be initiated by extracellular or intracellular stimuli, leading to the activation of caspases and subsequent cell death. A better understanding of the process of apoptosis in the heart is clearly important as it may lead to the identification of novel therapies for cardiovascular disease. This review is focused on the basic cellular mechanisms of apoptosis, as well as our current understanding of this process in the heart.
authors.affiliation: Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, California 92037, USA.
authors.forename: Asa B
authors.initials: AB
authors.lastname: Gustafsson
authors.forename: Roberta A
authors.initials: RA
authors.lastname: Gottlieb
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D002118:Calcium / Q000378:metabolism; D020169:Caspases / Q000378:metabolism; D006801:Humans; D020935:MAP Kinase Signaling System / Q000502:physiology; D008929:Mitochondria, Heart / Q000378:metabolism*; D009206:Myocardium / Q000166:cytology / Q000378:metabolism*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology*
chemical_list: D019253:Proto-Oncogene Proteins c-bcl-2; D017382:Reactive Oxygen Species; D020169:Caspases; D002118:Calcium