帕金森病中的自噬途径与关键药物靶点  

Autophagy pathways and key drug targets in Parkinson's disease

作　　者：欧阳亮[1] 张岚[1] 刘博[1] 

机构地区：[1]四川大学华西医院,生物治疗国家重点实验室,生物治疗协同创新中心,四川成都610041

出　　处：《药学学报》2016年第1期9-17,共9页Acta Pharmaceutica Sinica

基　　金：国家自然科学基金资助项目(81473091,81260628)

摘　　要：帕金森病(PD)是一种常见的神经退行性疾病。在过去几十年中,对PD的发病机制的探索已有了较大的进步,环境因素和遗传因素都会导致PD的发生,然而它的具体发病机制仍然未知。最近的研究表明自噬过程或许与PD密切相关,在许多PD患者和动物模型中都观察到了异常的自噬水平。此外,一些PD相关蛋白,如α-synuclein、Parkin和PINK1等都被发现参与自噬的调控,被认为与PD的发病机制相关。本文综述了几种重要PD相关蛋白在自噬途径中的作用,同时概述了通过调节自噬过程来治疗PD的潜在策略。Parkinson＇s disease（PD） is a common neurodegenerative disorder associated with aging. Great progresses have been made toward understanding the pathogenesis over the past decades. It seems that both genetic factors and environmental factors contribute to PD, while the precise pathogenesis still remains unknown. Recently, increasing evidence has suggested that autophagy dysregulation is closely related to PD. Dysregulation of the autophagic pathways has been observed in the brains of PD patients or in animal models of PD, and a number of PD-associated proteins, such as α-synuclein, Parkin and PINK1, were found to involve in autophagy, suggesting a link between autophagy and pathogenesis of PD. In this review, we summarized the role of PD-associated proteins in autophagy pathways. In addition, we described the efficacy of autophagy-modulating compounds in PD models and discussed promising strategies for PD therapy.

关 键 词：自噬 帕金森病 Α-突触核蛋白 线粒体自噬 帕金森病治疗 

分 类 号：R966[医药卫生—药理学]