Role of Mitophagy in Coronary Heart Disease: Targeting the Mitochondrial Dysfunction and Inflammatory Regulation

Coronary heart disease (CHD) is one of the main causes of death worldwide. In the past few decades, several in-depth research on the pathological mechanisms and effective treatment methods for CHD have been conducted. At present, the intervention of a variety of therapeutic drugs and treatment technologies have greatly reduced the burden on global public health. However, severe arrhythmia and myocardial fibrosis accompanying CHD in the later stages need to be addressed urgently. Mitochondria are important structural components for energy production and the main sites for aerobic respiration in cells. Mitochondria are involved in arrhythmia, myocardial fibrosis, and acute CHD and play a crucial role in regulating myocardial ischemia/hypoxia. Mitochondrial dysfunction or mitophagy disorders (including receptor-dependent mitophagy and receptor-independent mitophagy) play an important role in the pathogenesis of CHD, especially mitophagy. Mitophagy acts as a mediator in the inflammatory damage of cardiomyocytes or vascular endothelial cells and can clear mitochondria or organelles damaged by inflammation under normal conditions. We reviewed experimental advances providing evidence that mitochondrial homeostasis or mitochondrial quality control are important in the pathological mechanism of CHD. Further, we reviewed and summarized relevant regulatory drugs that target mitochondrial function and quality control.

Automated summary

Coronary heart disease (CHD) is a leading cause of death globally. The pathogenesis of CHD involves mitochondrial dysfunction and mitophagy disorders, which play crucial roles in regulating myocardial ischemia/hypoxia. Maintaining mitochondrial homeostasis and quality control are essential in understanding the pathological mechanism of CHD.