title: Having a change of heart: reversing the suicidal proclivities of cardiac myocytes.
abstract: The molecular and cellular basis for cardiac remodeling have been difficult to establish. Transcriptional analysis and genetic manipulation of the mouse heart have revealed expression of a molecular program for cardiac myocyte suicide under conditions of myocardial injury or hemodynamic stress. Interrupting the cardiomyocyte suicide program by selective ablation of inducible apoptosis genes has proven to be remarkably effective in preventing remodeling and heart failure following myocardial infarction. Since these apoptotic genes are similarly dysregulated in human heart disease, the stage is set for a new era of therapeutics targeting cardiac suicide genes and their products.
authors.affiliation: Washington University Center for Pharmacogenomics, 660 S. Euclid Ave., Campus Box 8086, St. Louis, MO 63110, USA. gdorn@dom.wustl.edu
authors.forename: Gerald W
authors.initials: GW
authors.lastname: Dorn
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000235:genetics*; D006801:Humans; D008565:Membrane Proteins / Q000235:genetics / Q000502:physiology; D051379:Mice; D008822:Mice, Transgenic; D024101:Mitochondrial Proteins / Q000235:genetics / Q000502:physiology; D008955:Models, Cardiovascular; D009203:Myocardial Infarction / Q000235:genetics / Q000473:pathology / Q000503:physiopathology; D032383:Myocytes, Cardiac / Q000473:pathology* / Q000502:physiology; D018377:Neurotransmitter Agents / Q000502:physiology; D015533:Transcriptional Activation; D020257:Ventricular Remodeling / Q000235:genetics / Q000502:physiology
chemical_list: D008565:Membrane Proteins; D024101:Mitochondrial Proteins; D018377:Neurotransmitter Agents; C501741:Nix protein, mouse