The Role of Mitochondrial Quality Control in Cardiac Ischemia/Reperfusion Injury

Figure 1

Injury mechanism involved in mitochondria at different stages of myocardial ischemia-reperfusion. Ischemia/reperfusion (IR) injury is divided into two stages, ischemia and reperfusion. Both involve a decline in ATP synthesis. In the phase of ischemia, the damaged mitochondrial respiratory chain will reduce ATP synthesis, coupled with continuous energy consumption of other tissues and organelles, resulting in a significant decrease in ATP content. Due to a lack of energy supply and increased vascular permeability, myocardial ischemia can cause temporary tissue damage. In the reperfusion phase, in addition to the continuous decline of ATP synthesis, the mitochondrial respiratory chain will also excessively produce ROS. ROS mediates prolonged mPTP opening that forms a channel to release cytochrome c and then activate the apoptotic cascade of cardiomyocytes, which further aggravates tissue damage.