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A prolonged period of ischemia leads to death of cardiac myocyte (myocardial infarction). In theory, quicker restoration of blood supply to the ischemic myocardium should reduce the extent of myocardial injury. However, reperfusion itself has the potential to exacerbate myocardial damage, a phenomenon known as reperfusion injury. Mitochondrial dysfunction plays a central role in mediating myocardial cell death by ischemia/reperfusion (IR). In particular, opening of the mitochondria permeability transition pore (mPTP) has been attributed to irreversible cell damage1, 2. Studies on the effects of preconditioning and postconditioning have revealed a number of signaling cascades that afford cardioprotection involving the mitochondria. Among them, inhibition of glycogen synthase kinase-3 (GSK-3) has been causatively related by many investigators to the protective effects of ischemic preconditioning3, 4, pharmacological preconditioning5, anesthetic postconditioning6, ischemic postconditioning7, and many chemical cardioprotective interventions8-13. However, some controversies exist regarding the involvement of GSK-3 inhibition in the ischemic preconditioning and postconditioning effects observed in mice14.

Overcoming an Energy Crisis?