线粒体复合体Ⅰ在帕金森病发病过程中作用的研究进展  

Research progress on the role of mitochondrial complex I in the pathogenesis of Parkinson's disease

作　　者：尹香 孙诚 YIN Xiang;SUN Cheng(Key Laboratory for Neuroregeneration,Co-Innovation Center of Neuroregeneration,Nantong University,Nantong 226001,China)

机构地区：[1]南通大学神经再生重点实验室,神经再生协同创新中心,南通226001

出　　处：《生理学报》2025年第1期167-180,共14页Acta Physiologica Sinica

基　　金：National Natural Science Foundation of China(No.3227193);Jiangsu Province Graduate Research and Practice Innovation Program(No.KYCX23-3383)。

摘　　要：当前,帕金森病(Parkinson's disease,PD)患病率持续上升。越来越多的证据表明,线粒体功能障碍在PD病因学中起着至关重要的作用,而线粒体复合体Ⅰ(mitochondrial complexⅠ,MCI)功能障碍是导致线粒体功能障碍最关键的因素之一。MCI功能障碍刺激多巴胺能神经元产生活性氧(reactive oxygen species,ROS),同时降低多巴胺能神经元活性和ATP生成,从而促进PD的病理进展。本文综述MCI在PD发病过程中作用的研究进展,以及基于MCI的PD治疗策略。Currently,the incidence of Parkinson's disease(PD)is on the rise.More and more evidences suggest that mitochondrial dysfunction plays a crucial role in the etiology of PD,and dysfunction of mitochondrial complex I(MCI)is one of the most critical factors leading to mitochondrial dysfunction.On one hand,MCI dysfunction stimulates dopaminergic neurons to produce reactive oxygen species(ROS).On the other hand,MCI dysfunction decreases dopaminergic neuron viability and reduces ATP production.All these outcomes promote the pathological progression of PD.This review summarizes research progress on the role of MCI in the pathogenesis of PD,as well as PD treatment strategies based on MCI.

关 键 词：帕金森病 线粒体复合体Ⅰ 线粒体功能障碍 Α-突触核蛋白 神经炎症 氧化应激 

分 类 号：R742.5[医药卫生—神经病学与精神病学]