The Role of Ubiquitin-Proteasome System and Mitophagy in the Pathogenesis of Parkinson's Disease.

IF 3.3 4区医学 Q2 NEUROSCIENCES NeuroMolecular Medicine Pub Date : 2023-12-01 Epub Date: 2023-09-12 DOI:10.1007/s12017-023-08755-0

Yu Liang, Guangshang Zhong, Mingxin Ren, Tingting Sun, Yangyang Li, Ming Ye, Caiyun Ma, Yu Guo, Changqing Liu

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引用次数: 1

Abstract

Parkinson's disease (PD) is a common neurodegenerative disease that is mainly in middle-aged people and elderly people, and the pathogenesis of PD is complex and diverse. The ubiquitin-proteasome system (UPS) is a master regulator of neural development and the maintenance of brain structure and function. Dysfunction of components and substrates of this UPS has been linked to neurodegenerative diseases such as Parkinson's disease and Alzheimer's disease. Moreover, UPS can regulate α-synuclein misfolding and aggregation, mitophagy, neuroinflammation and oxidative stress to affect the development of PD. In the present study, we review the role of several related E3 ubiquitin ligases and deubiquitinating enzymes (DUBs) on the pathogenesis of PD such as Parkin, CHIP, USP8, etc. On this basis, we summarize the connections and differences of different E3 ubiquitin ligases in the pathogenesis, and elaborate on the regulatory progress of different DUBs on the pathogenesis of PD. Therefore, we can better understand their relationships and provide feasible and valuable therapeutic clues for UPS-related PD treatment research.

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泛素-蛋白酶体系统和丝裂噬在帕金森病发病机制中的作用

帕金森病（Parkinson's disease，PD）是一种常见的神经退行性疾病，主要发病于中老年人，其发病机制复杂多样。泛素-蛋白酶体系统（UPS）是神经发育和大脑结构与功能维持的主调节器。泛素-蛋白酶体系统成分和底物的功能障碍与帕金森病和阿尔茨海默病等神经退行性疾病有关。此外，UPS 还能调节α-突触核蛋白的错误折叠和聚集、有丝分裂、神经炎症和氧化应激，从而影响帕金森病的发展。在本研究中，我们综述了几种相关的E3泛素连接酶和去泛素化酶（DUBs）在帕金森病发病机制中的作用，如Parkin、CHIP、USP8等。在此基础上，我们总结了不同E3泛素连接酶在发病机制中的联系和区别，并阐述了不同DUBs对帕金森病发病机制的调控过程。因此，我们可以更好地理解它们之间的关系，为UPS相关的PD治疗研究提供可行且有价值的治疗线索。

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来源期刊

NeuroMolecular Medicine 医学-神经科学

CiteScore

7.10

自引率

0.00%

发文量

审稿时长

>12 weeks

期刊介绍： NeuroMolecular Medicine publishes cutting-edge original research articles and critical reviews on the molecular and biochemical basis of neurological disorders. Studies range from genetic analyses of human populations to animal and cell culture models of neurological disorders. Emerging findings concerning the identification of genetic aberrancies and their pathogenic mechanisms at the molecular and cellular levels will be included. Also covered are experimental analyses of molecular cascades involved in the development and adult plasticity of the nervous system, in neurological dysfunction, and in neuronal degeneration and repair. NeuroMolecular Medicine encompasses basic research in the fields of molecular genetics, signal transduction, plasticity, and cell death. The information published in NEMM will provide a window into the future of molecular medicine for the nervous system.