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.