Abstract

Acute myocardial infarction has a rapid onset, is severe and has a high mortality rate that seriously threatens the lives of the population. Coronary intervention combined with drug treatment can open the criminal blood vessel and save the patient's life, but the surviving patient is not "cured" but must go through the process of myocardial ischemia reperfusion injury. Myocardial cells are end-stage cells and death of myocardial cells due to myocardial ischemia reperfusion injury irreversibly damages the structure and function of the heart. In the past, apoptosis was thought to be the only regulated form of cell death, whereas cell necrosis was not. However, recent studies suggest that cell necrosis can also be regulated, which is grouped under the term programmed cell death. Since regulated cell death is actively mediated by molecular signaling pathways, there is a possibility to inhibit this signaling and thus attenuate programmed cell death myocardial ischemia reperfusion injury. Currently, programmed cell death mainly includes apoptosis, autophagy, pyroptosis, necroptosis, and ferroptosis. In this paper, we explore the relationship between programmed cell death and myocardial ischemic reperfusion injury, in order to support the prevention and treatment of myocardial ischemic reperfusion injury by intervening in the perspective of programmed cell death.