title: Mechanisms of cell death in heart disease.
abstract: The major cardiac syndromes, myocardial infarction and heart failure, are responsible for a large portion of deaths worldwide. Genetic and pharmacological manipulations indicate that cell death is an important component in the pathogenesis of both diseases. Cells die primarily by apoptosis or necrosis, and autophagy has been associated with cell death. Apoptosis has long been recognized as a highly regulated process. Recent data indicate that a significant subset of necrotic deaths is also programmed. In the review, we discuss the molecular mechanisms that underlie these forms of cell death and their interconnections. The possibility is raised that small molecules aimed at inhibiting cell death may provide novel therapies for these common and lethal heart syndromes.
authors.affiliation: Department of Medicine, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
authors.forename: Klitos
authors.initials: K
authors.lastname: Konstantinidis
authors.forename: Russell S
authors.initials: RS
authors.lastname: Whelan
authors.forename: Richard N
authors.initials: RN
authors.lastname: Kitsis
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D017209:Apoptosis; D001343:Autophagy; D004721:Endoplasmic Reticulum / Q000502:physiology; D006331:Heart Diseases / Q000473:pathology*; D006333:Heart Failure / Q000473:pathology; D006801:Humans; D033681:Mitochondrial Membrane Transport Proteins; D000083162:Mitochondrial Permeability Transition Pore; D009203:Myocardial Infarction / Q000473:pathology; D009336:Necrosis; D017382:Reactive Oxygen Species / Q000378:metabolism; D053422:Receptor-Interacting Protein Serine-Threonine Kinases / Q000502:physiology
chemical_list: D033681:Mitochondrial Membrane Transport Proteins; D000083162:Mitochondrial Permeability Transition Pore; D017382:Reactive Oxygen Species; D000255:Adenosine Triphosphate; D053422:Receptor-Interacting Protein Serine-Threonine Kinases