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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 |
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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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