Luo Ai-Di, Xu Zu-Cai, Liao Shu-Sheng
Department of Neurology The Affiliated Hospital of Zunyi Medical University Zunyi Guizhou China.
Ibrain. 2021 Dec 9;7(4):318-324. doi: 10.1002/ibra.12004. eCollection 2021 Winter.
Parkinson's disease (PD) is a neurodegenerative disease that is common in middle-aged and elderly people, and its onset is related to multiple factors, such as heredity, environment, and age. The vesicle protein sorting 35 (VPS35) gene was found to be a late-onset autosomal dominant familial PD (PARK17) causative gene. The protein encoded by this gene is located in the endosome and aggregates with other membrane proteins to form a retromer complex, which participates in the membrane protein cycle between the endosome and the Golgi network. Increasing evidence shows that VPS35 may participate in the pathogenesis of PD by affecting autophagy, mitochondria, neurosynaptic transmission, dopamine signaling pathways, and so forth, and it can interact with other disease-causing genes of familial PD. This article aimed to review the functions of VPS35 and the mechanism of its mutations in PD that have been discovered in recent years.
帕金森病（PD）是一种在中老年人群中常见的神经退行性疾病，其发病与多种因素有关，如遗传、环境和年龄等。囊泡蛋白分选35（VPS35）基因被发现是迟发性常染色体显性家族性帕金森病（PARK17）的致病基因。该基因编码的蛋白质位于内体中，并与其他膜蛋白聚集形成逆向转运复合物，参与内体与高尔基体网络之间的膜蛋白循环。越来越多的证据表明，VPS35可能通过影响自噬、线粒体、神经突触传递、多巴胺信号通路等参与帕金森病的发病机制，并且它可以与家族性帕金森病的其他致病基因相互作用。本文旨在综述近年来发现的VPS35的功能及其在帕金森病中的突变机制。
