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多发性硬化症和实验性自身免疫性脑脊髓炎中的自噬调节。

Autophagy modulation in multiple sclerosis and experimental autoimmune encephalomyelitis.

机构信息

Department of Neurology, Qingdao Municipal Hospital, Qingdao 266000, Shan Dong Province, China.

Department of Stomatology, Qingdao Municipal Hospital, Qingdao 266000, Shan Dong Province, China.

出版信息

Clin Exp Immunol. 2022 Aug 19;209(2):140-150. doi: 10.1093/cei/uxac017.

DOI:10.1093/cei/uxac017
PMID:35641229
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9390842/
Abstract

Multiple sclerosis (MS), a white matter demyelinating disease of the central nervous system (CNS), is characterized by neuroinflammatory and neurodegenerative. Experimental autoimmune encephalomyelitis (EAE) is a commonly used animal model for investigating pathogenic mechanisms of MS, representing the destruction of the blood-brain barrier (BBB), the activation of T cells, and the infiltration of myeloid cells. An increasing number of studies have documented that autophagy plays a critical role in the pathogenesis of both MS and EAE. Autophagy maintains CNS homeostasis by degrading the damaged organelles and abnormal proteins. Furthermore, autophagy is involved in inflammatory responses by regulating the activation of immune cells and the secretion of inflammatory factors. However, the specific mechanisms of autophagy involved in MS and EAE are not completely understood. In this review, we will summarize the complex mechanisms of autophagy in MS and EAE, providing potential therapeutic approaches for the management of MS.

摘要

多发性硬化症(MS)是一种中枢神经系统(CNS)的白质脱髓鞘疾病,其特征是神经炎症和神经退行性变。实验性自身免疫性脑脊髓炎(EAE)是一种常用于研究 MS 发病机制的动物模型,代表血脑屏障(BBB)的破坏、T 细胞的激活和髓样细胞的浸润。越来越多的研究表明,自噬在 MS 和 EAE 的发病机制中起着关键作用。自噬通过降解受损的细胞器和异常蛋白来维持中枢神经系统的稳态。此外,自噬通过调节免疫细胞的激活和炎症因子的分泌参与炎症反应。然而,自噬在 MS 和 EAE 中的具体机制尚不完全清楚。在这篇综述中,我们将总结自噬在 MS 和 EAE 中的复杂机制,为 MS 的治疗提供潜在的治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a94/9390842/a6e237555aba/uxac017f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a94/9390842/a6e237555aba/uxac017f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a94/9390842/a6e237555aba/uxac017f0003.jpg

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