Hemostatic factors in the pathogenesis of neuroinflammation in multiple sclerosis.

IF 5

Multiple sclerosis (Houndmills, Basingstoke, England) Pub Date : 2022-10-01 Epub Date: 2021-08-19 DOI:10.1177/13524585211039111

Gianmarco Abbadessa, Luigi Lavorgna, Constantina Andrada Treaba, Simona Bonavita, Caterina Mainero

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引用次数: 6

Abstract

Background: A growing body of evidence has shed light on the role of the hemostatic pathway and its components in the pathogenesis of multiple sclerosis (MS), particularly in enhancing and sustaining neuroinflammation.

Objective: To review the clinical, experimental, and neuroimaging evidence supporting the role of different components of the hemostatic pathway in the pathogenesis of neuroinflammation in MS and discuss their translational potential as disease biomarkers and therapeutic targets.

Methods: A literature search for most relevant articles from 1956 to 2020 was conducted in PubMed and Scopus.

Results: Hemostasis components appear to be involved in different key events of neuroinflammation in MS including mononuclear cell diapedesis, microglia activation, and neuronal damage.

Conclusion: The findings on the interplay between hemostatic and thrombotic molecular pathways in the pathogenesis of neuroinflammation in MS open new opportunities for developing novel biomarkers for disease monitoring and prognosis, as well as novel therapeutic targets.

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止血因子在多发性硬化症神经炎症发病机制中的作用。

背景:越来越多的证据揭示了止血途径及其成分在多发性硬化症(MS)发病机制中的作用，特别是在增强和维持神经炎症方面。目的:回顾支持止血途径不同组分在多发性硬化症神经炎症发病机制中的作用的临床、实验和神经影像学证据，并讨论它们作为疾病生物标志物和治疗靶点的转化潜力。方法:在PubMed和Scopus中检索1956 ~ 2020年最相关的文献。结果:止血成分似乎参与了多发性硬化症神经炎症的不同关键事件，包括单核细胞脱落、小胶质细胞激活和神经元损伤。结论:MS神经炎症发病机制中止血和血栓分子通路相互作用的发现为开发新的疾病监测和预后生物标志物以及新的治疗靶点开辟了新的机会。

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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Multiple sclerosis (Houndmills, Basingstoke, England)

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