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α-突触核蛋白与 NLRP3 炎性小体在帕金森病中的相互作用。

The interplay between α-Synuclein and NLRP3 inflammasome in Parkinson's disease.

机构信息

School of Medicine and Holistic Integrative Medicine, Nanjing University of Chinese Medicine, Nanjing 210023, China.

Department of Pharmacology, Nanjing Medical University, Jiangsu 211166, China.

出版信息

Biomed Pharmacother. 2023 Dec;168:115735. doi: 10.1016/j.biopha.2023.115735. Epub 2023 Oct 16.

Abstract

α-Synuclein is a member of a protein of synucleins, which is a presynaptic neuron protein. It is usually highly expressed in the brain and participates in the formation and transmission of nerve synapses. It has been reported that abnormal aggregation of α-Syn can induce the activation of NLRP3 inflammasome in microglia, increase the production of IL-1β, and aggravate neuroinflammation. Therefore, it is recognized as one of the important factors leading to neuroinflammation in Parkinson's disease. In this paper, we aimed to explore the influence of post-translational modification of α-Syn on its pathological aggregation and summarize various pathways that activate NLRP3 triggered by α-Syn and targeted therapeutic strategies, which provided new insights for further exploring the origin and targeted therapy of Parkinson's disease.

摘要

α-突触核蛋白是突触核蛋白家族的一员,它是一种突触前神经元蛋白。它通常在大脑中高度表达,并参与神经突触的形成和传递。有报道称,α-突触核蛋白的异常聚集可诱导小胶质细胞中 NLRP3 炎性体的激活,增加 IL-1β 的产生,并加重神经炎症。因此,它被认为是导致帕金森病神经炎症的重要因素之一。本文旨在探讨 α-突触核蛋白翻译后修饰对其病理性聚集的影响,并总结激活 α-突触核蛋白触发的 NLRP3 的各种途径和靶向治疗策略,为进一步探讨帕金森病的发病机制和靶向治疗提供新的思路。

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