Abstract

Cardiovascular disease has become one of the main causes of human death. In addition, many cardiovascular diseases are accompanied by a series of irreversible damages that lead to organ and vascular complications. In recent years, the potential therapeutic strategy of natural antioxidants in the treatment of cardiovascular diseases through mitochondrial quality control has received extensive attention. Mitochondria are the main site of energy metabolism in eukaryotic cells, including myocardial and vascular endothelial cells. Mitochondrial quality control processes ensure normal activities of mitochondria and cells by maintaining stable mitochondrial quantity and quality, thus protecting myocardial and endothelial cells against stress. Various stresses can affect mitochondrial morphology and function. Natural antioxidants extracted from plants and natural medicines are becoming increasingly common in the clinical treatment of diseases, especially in the treatment of cardiovascular diseases. Natural antioxidants can effectively protect myocardial and endothelial cells from stress-induced injury by regulating mitochondrial quality control, and their safety and effectiveness have been preliminarily verified. This review summarises the damage mechanisms of various stresses in cardiomyocytes and vascular endothelial cells and the mechanisms of natural antioxidants in improving the vulnerability of these cell types to stress by regulating mitochondrial quality control. This review is aimed at paving the way for novel treatments for cardiovascular diseases and the development of natural antioxidant drugs.

Highlights

  • Mitochondria are double-membrane-bound organelles that play an important role in the energy homeostasis of eukaryotic cells, including cardiomyocytes and endothelial cells [1]

  • Ischaemia, hypoxia, inflammation, and other stress conditions, mitochondrial homeostasis is disrupted [5]. This results in a disbalance of mitochondrial quality control (MQC), which affects mitochondrial quality and quantity, which can further lead to mitochondrial dysfunction and enhanced vulnerability, Oxidative Medicine and Cellular Longevity and induce apoptosis in cells [6, 7]

  • The mammalian mitochondrial genome has 37 genes, 13 of which encode polypeptide subunits of enzyme complexes of the oxidative phosphorylation system, which provides more than 95% of the myocardial energy requirement for adenosine triphosphate (ATP) production [16, 17]

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Summary

Introduction

Mitochondria are double-membrane-bound organelles that play an important role in the energy homeostasis of eukaryotic cells, including cardiomyocytes and endothelial cells [1]. With changes in the physiological environment, mitochondria can perform specific physiological processes related to quantity, morphology, and quality to maintain their structure and function. This process, termed “mitochondrial homeostasis,” is an important prerequisite for mitochondrial quality control (MQC) [3, 4]. Ischaemia, hypoxia, inflammation, and other stress conditions, mitochondrial homeostasis is disrupted [5] This results in a disbalance of MQC, which affects mitochondrial quality and quantity, which can further lead to mitochondrial dysfunction and enhanced vulnerability, Oxidative Medicine and Cellular Longevity and induce apoptosis in cells [6, 7]. MQC can be regulated by natural antioxidants in the treatment of CVDs and can further maintain the normal function of mitochondria

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