神经炎症:少突中心的观点。

IF 5.1 2区 医学 Q1 NEUROSCIENCES Glia Pub Date : 2025-03-10 DOI:10.1002/glia.70007
Lindsay K. Festa, Kelly L. Jordan-Sciutto, Judith B. Grinspan
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引用次数: 0

摘要

慢性神经炎症是一系列神经系统疾病的重要病理机制,由中枢神经系统(CNS)驻留的星形胶质细胞和小胶质细胞以及外周免疫系统的浸润驱动。几十年来,研究几乎完全集中在神经炎症如何影响神经元功能;然而,越来越多的证据表明,对少突胶质细胞谱系的损伤是病理和临床结果的重要组成部分。虽然少突胶质细胞能够进行内源性修复过程,即髓鞘再生,但这一过程变得低效,通常在持续炎症的情况下失败。目前的综述集中在我们目前对慢性脱髓鞘疾病、多发性硬化症中先天和适应性免疫系统激活的了解,并提供证据表明,在其他神经系统疾病中,如围产期白质损伤、创伤性脑损伤和病毒感染,持续的神经炎症集中在少突胶质细胞损伤上。最后,讨论了针对炎症对这些疾病的少突胶质细胞谱系的影响的治疗潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Neuroinflammation: An Oligodendrocentric View

Chronic neuroinflammation, driven by central nervous system (CNS)-resident astrocytes and microglia, as well as infiltration of the peripheral immune system, is an important pathologic mechanism across a range of neurologic diseases. For decades, research focused almost exclusively on how neuroinflammation impacted neuronal function; however, there is accumulating evidence that injury to the oligodendrocyte lineage is an important component for both pathologic and clinical outcomes. While oligodendrocytes are able to undergo an endogenous repair process known as remyelination, this process becomes inefficient and usually fails in the presence of sustained inflammation. The present review focuses on our current knowledge regarding activation of the innate and adaptive immune systems in the chronic demyelinating disease, multiple sclerosis, and provides evidence that sustained neuroinflammation in other neurologic conditions, such as perinatal white matter injury, traumatic brain injury, and viral infections, converges on oligodendrocyte injury. Lastly, the therapeutic potential of targeting the impact of inflammation on the oligodendrocyte lineage in these diseases is discussed.

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来源期刊
Glia
Glia 医学-神经科学
CiteScore
13.10
自引率
4.80%
发文量
162
审稿时长
3-8 weeks
期刊介绍: GLIA is a peer-reviewed journal, which publishes articles dealing with all aspects of glial structure and function. This includes all aspects of glial cell biology in health and disease.
期刊最新文献
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