Tan Ying, Xia Fengfan, Li Lulan, Peng Xiaojie, Liu Wenqian, Zhang Yaoyuan, Fang Haihong, Zeng Zhenhua, Chen Zhongqing
Department of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Department of Cardiology, Shunde Hospital, Southern Medical University (The First People's Hospital of Shunde Foshan), Foshan, 528300 Guangdong, China.
Oxid Med Cell Longev. 2021 Feb 20;2021:6669075. doi: 10.1155/2021/6669075. eCollection 2021.
Mitochondria maintain mitochondrial homeostasis through continuous fusion and fission, that is, mitochondrial dynamics, which is precisely mediated by mitochondrial fission and fusion proteins, including dynamin-related protein 1 (Drp1), mitofusin 1 and 2 (Mfn1/2), and optic atrophy 1 (OPA1). When the mitochondrial fission and fusion of cardiomyocytes are out of balance, they will cause their own morphology and function disorders, which damage the structure and function of the heart, are involved in the occurrence and progression of cardiovascular disease such as ischemia-reperfusion injury (IRI), septic cardiomyopathy, and diabetic cardiomyopathy. In this paper, we focus on the latest findings regarding the molecular features and regulatory mechanisms of mitochondrial dynamic disorder in cardiovascular pathologies. Finally, we will address how these findings can be applied to improve the treatment of cardiovascular disease.
线粒体通过持续的融合和裂变来维持线粒体稳态，即线粒体动力学，这一过程由线粒体裂变和融合蛋白精确介导，包括动力相关蛋白1（Drp1）、线粒体融合蛋白1和2（Mfn1/2）以及视神经萎缩蛋白1（OPA1）。当心肌细胞的线粒体裂变和融合失衡时，会导致其自身形态和功能紊乱，损害心脏的结构和功能，参与缺血再灌注损伤（IRI）、脓毒症性心肌病和糖尿病性心肌病等心血管疾病的发生和发展。在本文中，我们聚焦于心血管疾病中线粒体动力学紊乱的分子特征和调控机制的最新研究发现。最后，我们将探讨如何应用这些发现来改善心血管疾病的治疗。
