Acute induction of autophagy as a novel strategy for cardioprotection: Getting to the heart of the matter

Karin Przyklenk, Vishnu Vardhan Reddy Undyala, Joseph Wider, Javier A. Sala-Mercado, Roberta A. Gottlieb, Robert M. Mentzer

Research output: Contribution to journalShort surveypeer-review

47 Scopus citations

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 provide 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.

Original languageEnglish
Pages (from-to)432-433
Number of pages2
JournalAutophagy
Volume7
Issue number4
DOIs
StatePublished - Apr 2011

Keywords

  • Autophagy
  • Chloramphenicol
  • Ischemia-reperfusion injury
  • Myocardial infarction
  • Myocardial ischemia

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