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Role of Mitophagy in Coronary Heart Disease: Targeting the Mitochondrial Dysfunction and Inflammatory Regulation
1School of Nursing, Capital Medical University, Beijing, China.
Insights
Mitochondrial dysfunction and mitophagy disorders are key in coronary heart disease (CHD) pathogenesis. Targeting mitochondrial quality control offers promising therapeutic strategies for treating CHD and its complications like arrhythmia and fibrosis.
Area of Science:
- Cardiovascular Medicine
- Cell Biology
- Mitochondrial Biology
Background:
- Coronary heart disease (CHD) remains a leading global cause of mortality.
- While treatments have improved, severe arrhythmia and myocardial fibrosis in later CHD stages require urgent attention.
- Mitochondria are crucial for cellular energy production and are implicated in myocardial ischemia/hypoxia, arrhythmia, and fibrosis.
Purpose of the Study:
- To review experimental evidence on the role of mitochondrial homeostasis and quality control in CHD pathogenesis.
- To summarize current therapeutic drugs targeting mitochondrial function and quality control for CHD.
Main Methods:
- Literature review of experimental advances in CHD research.
- Focus on the role of mitochondrial dysfunction and mitophagy in cardiovascular disease.
- Analysis of regulatory drugs targeting mitochondrial pathways.
Main Results:
- Mitochondrial dysfunction and mitophagy disorders are significant contributors to CHD.
- Mitophagy plays a critical role in mediating inflammatory damage and clearing damaged mitochondria in cardiomyocytes and vascular endothelial cells.
- Evidence supports the importance of maintaining mitochondrial homeostasis and quality control in CHD pathology.
Conclusions:
- Mitochondrial homeostasis and quality control are vital in the pathological mechanisms of CHD.
- Targeting mitochondrial function and quality control presents a promising therapeutic avenue for CHD, including managing associated arrhythmia and myocardial fibrosis.
Abstract:
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.
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