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


OBJECTIVE
Here we review the apoptotic and autophagic signaling pathways, their influences on each other, and we discuss the relevance of autophagy in the heart.
Hamacher-Brady
Anne
A
Department of Molecular and Experimental Medicine MEM-220, The Scripps Research Institute, 10550 N. Torrey Pines Road, La Jolla, San Diego, CA 92037, USA.
Brady
Nathan Ryan
NR
Gottlieb
Roberta Anne
RA
D017209:Apoptosis; D001343:Autophagy; D002470:Cell Survival; D006801:Humans; D008928:Mitochondria / Q000378:metabolism; D017202:Myocardial Ischemia / Q000378:metabolism / Q000503:physiopathology*; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000503:physiopathology*; D009206:Myocardium / Q000166:cytology / Q000378:metabolism; D032383:Myocytes, Cardiac / Q000166:cytology / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D015398:Signal Transduction
D019253:Proto-Oncogene Proteins c-bcl-2