title: Acute induction of autophagy as a novel strategy for cardioprotection: getting to the heart of the matter.
abstract: There is no question that necrosis and apoptosis contribute to cardiomyocyte death in the setting of myocardial ischemia-reperfusion. Indeed, considerable effort and resources have been invested in the development of novel therapies aimed at attenuating necrotic and apoptotic cell death, with the ultimate goal of applying these strategies to reduce infarct size and improve outcome in patients suffering acute myocardial infarction (MI) or 'heart attack'. However, an issue that remains controversial is the role of autophagy in determining the fate of ischemic-reperfused cardiomyocytes: i.e., is induction of autophagy detrimental or protective? Recent data from our group obtained in the clinically relevant, in vivo swine model of acute MI provides novel evidence of a positive association between pharmacological upregulation of autophagy (achieved by administration of chloramphenicol succinate (CAPS)) and increased resistance to myocardial ischemia-reperfusion injury.
authors.affiliation: Cardiovascular Research Institute, Wayne State University, Detroit, MI, USA. kprzykle@med.wayne.edu
authors.forename: Karin
authors.initials: K
authors.lastname: Przyklenk
authors.forename: Vishnu Vardhan Reddy
authors.initials: VV
authors.lastname: Undyala
authors.forename: Joseph
authors.initials: J
authors.lastname: Wider
authors.forename: Javier A
authors.initials: JA
authors.lastname: Sala-Mercado
authors.forename: Roberta A
authors.initials: RA
authors.lastname: Gottlieb
authors.forename: Robert M
authors.initials: RM
authors.lastname: Mentzer
mesh_terms: D000818:Animals; D017209:Apoptosis; D001343:Autophagy; D002701:Chloramphenicol / Q000031:analogs & derivatives / Q000494:pharmacology; D004195:Disease Models, Animal; D008954:Models, Biological; D015428:Myocardial Reperfusion Injury / Q000473:pathology; D009206:Myocardium / Q000378:metabolism; D032383:Myocytes, Cardiac / Q000166:cytology*; D009336:Necrosis / Q000378:metabolism; D010641:Phenotype; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D015398:Signal Transduction; D013552:Swine; D013997:Time Factors
chemical_list: D002701:Chloramphenicol; D019869:Phosphatidylinositol 3-Kinases; C026016:chloramphenicol succinate