The interplay between pro-death and pro-survival signaling pathways in myocardial ischemia/reperfusion injury: apoptosis meets autophagy

Cardiovasc Drugs Ther. 2006 Dec;20(6):445-62. doi: 10.1007/s10557-006-0583-7.

Abstract

Introduction: Programmed cell death of cardiac myocytes occurs following a bout of ischemia/reperfusion (I/R), which results in reduced function of the heart. Numerous studies, including in vivo, have shown that cell death occurs via necrosis and apoptosis following I/R. Recently, autophagy has emerged as a powerful mediator of programmed cell death, either opposing or enhancing apoptosis, or acting as an alternative form of programmed cell death distinct from apoptosis.

Aim: Here we review the apoptotic and autophagic signaling pathways, their influences on each other, and we discuss the relevance of autophagy in the heart.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Apoptosis*
  • Autophagy*
  • Cell Survival
  • Humans
  • Mitochondria / metabolism
  • Myocardial Ischemia / metabolism
  • Myocardial Ischemia / physiopathology*
  • Myocardial Reperfusion Injury / metabolism
  • Myocardial Reperfusion Injury / physiopathology*
  • Myocardium / cytology
  • Myocardium / metabolism
  • Myocytes, Cardiac / cytology
  • Myocytes, Cardiac / metabolism
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Signal Transduction*

Substances

  • Proto-Oncogene Proteins c-bcl-2