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DOI 10.1007/s12192-023-01384-3

Медицинская библиотека · Cell stress & chaperones · 2023

Roles of mitochondrial dynamics and mitophagy in diabetic myocardial microvascular injury.

Wang Tong, Wang Xinwei, Fu Tong, Ma Yanchun, Wang Qi, Zhang Shuxiang, Zhang Xiao, Zhou Hao, Chang Xing, Tong Ying

СтатьяОбзорПоддержка исследования: вне правительства СШАПеревод пока не подготовлен

Аннотация

Myocardial microvessels are composed of a monolayer of endothelial cells, which play a crucial role in maintaining vascular barrier function, luminal latency, vascular tone, and myocardial perfusion. Endothelial dysfunction is a key factor in the development of cardiac microvascular injury and diabetic cardiomyopathy. In addition to their role in glucose oxidation and energy metabolism, mitochondria also participate in non-metabolic processes such as apoptosis, intracellular ion handling, and redox balancing. Mitochondrial dynamics and mitophagy are responsible for regulating the quality and quantity of mitochondria in response to hyperglycemia. However, these endogenous homeostatic mechanisms can both preserve and/or disrupt non-metabolic mitochondrial functions during diabetic endothelial damage and cardiac microvascular injury. This review provides an overview of the molecular features and regulatory mechanisms of mitochondrial dynamics and mitophagy. Furthermore, we summarize findings from various investigations that suggest abnormal mitochondrial dynamics and defective mitophagy contribute to the development of diabetic endothelial dysfunction and myocardial microvascular injury. Finally, we discuss different therapeutic strategies aimed at improving endothelial homeostasis and cardiac microvascular function through the enhancement of mitochondrial dynamics and mitophagy.

Для цитирования: Wang Tong, Wang Xinwei, Fu Tong, Ma Yanchun, Wang Qi, Zhang Shuxiang, Zhang Xiao, Zhou Hao, Chang Xing, Tong Ying. Roles of mitochondrial dynamics and mitophagy in diabetic myocardial microvascular injury.. Cell stress & chaperones. 2023. DOI: 10.1007/s12192-023-01384-3.

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