NLRP3 炎症小体在缺血性中风发病机制中的作用

IF 0.6 4区生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY

Journal of Evolutionary Biochemistry and Physiology Pub Date : 2024-06-26 DOI:10.1134/s0022093024030098

S. D. Kazakov, E. M. Kamenskih, E. V. Udut

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引用次数: 0

摘要

摘要缺血性脑卒中（IS）是一种全球流行的疾病，具有很高的死亡率和致残风险。由于再灌注措施的有效性和安全性有限，其病因治疗问题至今仍未解决。最新研究阐明，神经炎症在 IS 的发生发展中起着关键作用，并可能成为治疗靶点。NLRP3 炎症小体是缺血后炎症反应的一个关键介质，它通过激活 caspase-1，将原-IL-1β 和原-IL-18 分解为活性促炎细胞因子释放到细胞外环境中。这篇综述深入探讨了 IS 中 NLRP3 炎症小体的结构和激活过程，概述了导致其激活和抑制的因素和机制。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

Role of NLRP3 Inflammasome in Pathogenesis of Ischemic Stroke

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Role of NLRP3 Inflammasome in Pathogenesis of Ischemic Stroke

Abstract

Ischemic stroke (IS) is a prevalent condition worldwide with high mortality and disability risks. The issue of its pathogenetic therapy remains unresolved by now due to the limited effectiveness and safety of reperfusion measures. Recent research has elucidated that neuroinflammation plays a pivotal role in IS development and may serve as a therapeutic target. The NLRP3 inflammasome emerges as a key mediator orchestrating post-ischemic inflammatory reactions through activation of caspase-1, which cleaves pro-IL-1β and pro-IL-18 into active pro-inflammatory cytokines released into the extracellular milieu. This review presents insights into the structure and activation process of the NLRP3 inflammasome in IS. The factors and mechanisms contributing to both its activation and inhibition are outlined.

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来源期刊

Journal of Evolutionary Biochemistry and Physiology 生物-进化生物学

自引率

33.30%

发文量

110

审稿时长

6-12 weeks

期刊介绍： Journal of Evolutionary Biochemistry and Physiology publishes original experimental and theoretical and review articles related to evolution of the main forms of metabolism in connection with life origin; comparative and ontogenetic physiology and biochemistry, biochemical evolution of animal world; as well as evolution of functions; morphology, pharmacology, pathophysiology and ecological physiology. The journal welcomes manuscripts from all countries in the English or Russian language.