Editorial

Nearly 3 decades ago, this journal reported the seminal discovery by Murry et al1 of ischemic precondition-ing, a phenomenon in which several episodes of brief isch-emia followed by reperfusion protected cardiac muscle cells from a subsequent prolonged ischemic insult. Since then, a similar protective effect of ischemic preconditioning has been observed in many organs, including brain, liver, and kidney, supporting the notion that ischemic preconditioning is a fun-damental property shared by different cell types. Given the obvious clinical implications, intense research efforts have been devoted to dissecting the mechanisms and identifying the putative mediators underlying the short-term or long-term cardioprotective effects induced by preconditioning.2 Different forms of nonischemic preconditioning have been demonstrated in the heart, including mechanical stretch, heat stress, metabolic challenge, and pharmacological agents.3,