Novel Molecular Targets Participating in Myocardial Ischemia-Reperfusion Injury and Cardioprotection

Figure 1

Conceptual diagram of the development and unknown mechanisms of myocardial ischemia-reperfusion injury. The pathophysiological nature of MIRI is the short-term disturbance of myocardial energy and metabolism caused by reflow after ischemia and hypoxia in the coronary artery and the dynamic changes in apoptosis and the prosurvival signaling pathways in response to related injury factors. During injury stimulation, the major effects on the cardiac function may be those involving mitochondria-dominated events along with potential nucleus-governed genetic/epigenetic alternations within the cardiomyocytes as well as the macrophage-led inflammation and T-cell-led immune responses underlying the myocardium-vessel interactive cascade. There are still many unknown aspects of MIRI's key molecular mechanisms that merit further study through both in vivo and in vitro MIRI models to discover novel functional molecular targets and identify associated cardioprotective mechanisms, which is important for improving the current treatment of AMI and MIRI. AMI, acute myocardial infarction; MIRI, myocardial ischemiareperfusion injury; ROS, reactive oxygen species; RNS, reactive nitrogen species; mPTP, mitochondrial permeability transition pore.