Advances in the regulation of mitochondrial dynamic Changes by MFN2
LIN Xiaoying1 HUANG Haofeng1 CHEN Hao2 LI Shupeng3 ZHAO Bin4 ZHONG Wangtao5 FENG Du1
1.Guangdong Medical University, Guangdong Province, Zhanjiang 524000, China;
2.Department of Neurology, the First Afiliated Hospital of Hainan Medical University, Hainan Province, Haikou 570100, China;
3.Department of Neurology, Zengcheng District People′s Hospital, Guangdong Province, Guangzhou 511300, China;
4.Guangdong Key Laboratory of Age-related Cardiac-Cerebral Vascular Disease, Institute of Neurology, the Afiliated Hospital of Guangdong Medical University, Guangdong Province, Zhanjiang 524000, China;
5.Department of Neurology, the Afiliated Hospital of Guangdong Medical University, Guangdong Province, Zhanjiang 524000, China
Abstract:To maintain mitochondria homeostasis, mitochondria remove damaged or excess mitochondria by autophagy. Mitochondria fission and fusion process is the basis of mitophagy, and mitofusion-2 (MFN2) is involved in the process of regulating mitochondria fission and fusion. Mutations in MFN2 could cause mitochondria dysfunction and even lead to neurodegenerative diseases such as Charcot-Marie-Tooth. This paper review recent research progress of MFN2 function and its effect on mitochondria autophagy and neurodegenerative disease, aiming at providing reference for further research in related fields.
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