Autophagy in myocardial ischemia and ischemia/reperfusion
Aleksandra Aljakna Khan, Sara Sabatasso
Abstract
• Autophagy plays a protective role in an in vivo animal model of permanent myocardial ischemia. • Autophagy is quickly induced by permanent myocardial ischemia (during initial 2 h) and after 4 hours localizes primarily in salvageable cardiomyocytes in the border zone. • Autophagy is further increased in an in vivo model of ischemia/reperfusion but via a different molecular mechanism and promotes myocardial injury. Myocardial infarction (MI) is a life-threatening condition that leads to loss of viable heart tissue. The best way to treat acute MI and limit the infarct size is to re-open the occluded coronary artery and restore the supply of oxygenated and nutrient-rich blood, but reperfusion can cause additional damage. Autophagy is an intracellular process that recycles damaged cytoplasmic components (molecules and organelles) by loading them into autophagosomes and degrading them in autolysosomes. Autophagy is increased in in vivo animal models of permanent ischemia and ischemia/reperfusion but by different molecular mechanisms. While autophagy is protective during permanent ischemia, it is detrimental during ischemia/reperfusion. Its modulation is being investigated as a potential target to reduce reperfusion injury. This review provides a synopsis of the current knowledge about autophagy, summarizes findings specifically in permanent ischemia and ischemia/reperfusion, and briefly discusses the potential implication of experimental findings.