Autophagy is the endogenous, tightly regulated cellular "housekeeping" process 
responsible for the degradation of damaged and dysfunctional cellular organelles 
and protein aggregates. There is a growing consensus that autophagy is 
upregulated in the setting of myocardial ischemia-reperfusion. Moreover, 
emerging data suggest that autophagy may serve as an adaptive process and confer 
increased resistance to ischemia-reperfusion injury. Our aims in this review are 
to (1) provide a brief synopsis of process of autophagy (including an overview 
of the key molecular mediators of this catabolic process and its relationship 
with other cardiac signaling pathways) and (2) most importantly, summarize the 
current evidence for versus against the intriguing concept of autophagy-mediated 
cardioprotection.