铜代谢异常在帕金森发病机制中的研究进展  

Research advances in the pathogenesis of abnormal copper metabolism in Parkinson’s disease

作　　者：杨慧捷 兰瑞 王漫漫[1] 王玮玮[1] 李泓宇 唐琛 刘双 杨杰丽 沈晓明 YANG Huijie;LAN Rui;WANG Manman;WANG Weiwei;LI Hongyu;TANG Chen;LIU Shuang;YANG Jieli;SHEN Xiaoming(Encephalopathy Center,the First Affiliated Hospital of Henan University of Chinese Medicine,Zhengzhou 450000,China;the First Clinical College of Medicine,Henan University of Chinese Medicine,Zhengzhou 450000)

机构地区：[1]河南中医药大学第一附属医院脑病中心,郑州450000 [2]河南中医药大学第一临床医学院,郑州450000

出　　处：《中国比较医学杂志》2024年第10期118-124,共7页Chinese Journal of Comparative Medicine

基　　金：国家自然科学基金(81973618,81503422);河南省中医药科学研究专项课题(2022JDZX090);河南省中医药科学研究专项课题(2019ZY1006);河南省自然科学基金(202300410399)。

摘　　要：帕金森病是一种与大脑铜代谢异常有关的神经退行性疾病,铜代谢异常导致α-突触核蛋白-铜络合物的错误折叠和聚集是帕金森病的重要病理标志。铜代谢是指有铜离子参与的细胞代谢过程,与帕金森病中α-突触核蛋白聚集、多巴胺代谢、线粒体功能障碍、氧化应激、铁死亡等发病机制密切相关。在本综述中,我们通过研究铜代谢异常在帕金森病中发挥病理作用的机制,描述铜发挥其毒性的分子代谢机制,以期为进一步完善作用机制和药物的开发提供依据和帮助。Parkinson's disease is a neurodegenerative disease associated with abnormal copper metabolism in the brain,which leads to misfolding and aggregation ofα-synuclein-copper complexes,which is an important pathological sign of Parkinson's disease.Copper metabolism,i.e.,cellular metabolic processes involving copper ions,is closely related to the pathogenesis ofα-synuclein aggregation,dopamine metabolism,mitochondrial dysfunction,oxidative stress,and ferroptosis in Parkinson's disease.In this review,we summarize the molecular metabolic mechanism of copper toxicity by studying the pathological role of copper metabolism in Parkinson's disease,to support our further understanding of the mechanism of action and drug development.

关 键 词：帕金森病 铜代谢 氧化应激 Α-突触核蛋白 铜蓝蛋白 线粒体功能障碍 

分 类 号：R-33[医药卫生]