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Nrf2在帕金森病中的作用:新视角探索

Role of Nrf2 in Parkinson's Disease: Toward New Perspectives.

作者信息

Yang Xin-Xing, Yang Rong, Zhang Feng

机构信息

Laboratory Animal Center and Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnomedicine of Ministry of Education and Key Laboratory of Basic Pharmacology of Guizhou Province, Zunyi Medical University, Zunyi, China.

Collaborative Innovation Center of Tissue Damage Repair and Regeneration Medicine of Zunyi Medical University, Zunyi, China.

出版信息

Front Pharmacol. 2022 Jun 24;13:919233. doi: 10.3389/fphar.2022.919233. eCollection 2022.

DOI:10.3389/fphar.2022.919233
PMID:35814229
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9263373/
Abstract

Parkinson's disease (PD) is one of the most common and chronic degenerative diseases in the central nervous system. The main pathology of PD formation is the progressive loss of dopaminergic neurons in substantia nigra and the formation of α-synuclein-rich Lewy bodies. The pathogenesis of PD is not caused by any single independent factor. The diversity of these independent factors of PD, such as iron accumulation, oxidative stress, neuroinflammation, mitochondrial dysfunction, age, environment, and heredity, makes the research progress of PD slow. Nrf2 has been well-known to be closely associated with the pathogenesis of PD and could regulate these induced factors development. Nrf2 activation could protect dopaminergic neurons and slow down the progression of PD. This review summarized the role of Nrf2 pathway on the pathogenesis of PD. Regulation of Nrf2 pathway might be one of the promising strategies to prevent and treat PD.

摘要

帕金森病(PD)是中枢神经系统最常见的慢性退行性疾病之一。PD形成的主要病理学特征是黑质中多巴胺能神经元的渐进性丧失以及富含α-突触核蛋白的路易小体的形成。PD的发病机制并非由任何单一独立因素引起。PD这些独立因素的多样性,如铁蓄积、氧化应激、神经炎症、线粒体功能障碍、年龄、环境和遗传等,使得PD的研究进展缓慢。众所周知,Nrf2与PD的发病机制密切相关,并且可以调节这些诱发因素的发展。Nrf2激活可以保护多巴胺能神经元并减缓PD的进展。本综述总结了Nrf2通路在PD发病机制中的作用。调节Nrf2通路可能是预防和治疗PD的有前景的策略之一。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6861/9263373/ec30a701b4c8/fphar-13-919233-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6861/9263373/631a64b9d1a5/fphar-13-919233-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6861/9263373/334ed808eb5f/fphar-13-919233-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6861/9263373/631a64b9d1a5/fphar-13-919233-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6861/9263373/334ed808eb5f/fphar-13-919233-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6861/9263373/441260cf36c9/fphar-13-919233-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6861/9263373/ec30a701b4c8/fphar-13-919233-g004.jpg

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