Cell Autophagy and Myocardial Ischemia/Reperfusion Injury

Ischemic heart disease is a clinical syndrome resulting from myocardial ischemia and is characterized by an imbalance between the supply and demand of myocardial blood flow and myocardial oxygen metabolism. It is currently one of the major diseases that endanger human health. Early and effective reconstruction of ischemic myocardial blood perfusion is the fundamental measure taken to prevent the development of ischemic myocardial injury, reduce myocardial infarct size, and improve the clinical prognosis. However, several studies have discovered that in some cases, reperfusion of ischemic cells could cause further injury in the form of ischemia/reperfusion injury. The clinical manifestations of myocardial ische‐ mia-reperfusion injury include arrhythmia, myocardial stunning, and no-reflow. Although lethal reperfusion injury in clinical practice is more difficult to identify, it is the most serious consequence of ischemia/reperfusion injury and is also the main reason preventing the is‐ chemic myocardium recovery from effective reperfusion therapy. Therefore, studies on the modes of myocardial cell death after ischemia/reperfusion are of great significance. Previous studies suggested that myocardial cell death following myocardial ischemia/reperfusion in‐ jury were mainly necrosis and apoptosis. Apoptosis receives more attention due to its death program. However, in recent years, a number of studies have suggested that, another proce‐ dural manner of death---autophagy, type II programmed cell death, also plays a critical role in ischemia/reperfusion injury. The study of this death pathway may provide a new effec‐ tive way to block myocardial ischemia/reperfusion injury. Therefore, in this chapter, the roles and possible mechanisms of autophagy in myocardial ischemia/reperfusion injury will be reviewed.