A brain in flame; do inflammasomes and pyroptosis influence stroke pathology?

被引:224
作者
Barrington, Jack [1 ]
Lemarchand, Eloise [1 ]
Allan, Stuart M. [1 ]
机构
[1] Univ Manchester, Fac Biol Med & Hlth, AV Hill Bldg,Oxford Rd, Manchester M13 9PT, Lancs, England
基金
英国医学研究理事会;
关键词
inflammation; inflammasome; interleukin-1; pyroptosis; NLRP3; ischemic stroke; hemorrhagic stroke; INTERLEUKIN-1-BETA CONVERTING-ENZYME; NLRP3; INFLAMMASOME; CELL-DEATH; SUBARACHNOID HEMORRHAGE; THROMBOEMBOLIC STROKE; TRANSIENT ISCHEMIA; DANGER SIGNAL; GASDERMIN D; ACTIVATION; INJURY;
D O I
10.1111/bpa.12476
中图分类号
R74 [神经病学与精神病学];
学科分类号
100204 [神经病学];
摘要
Stroke is one of the leading causes of death and disability worldwide. Inflammation plays a key role across the time course of stroke, from onset to the post-injury reparative phase days to months later. Several regulatory molecules are implicated in inflammation, but the most established inflammatory mediator of acute brain injury is the cytokine interleukin-1. Interleukin-1 is regulated by large, macromolecular complexes called inflammasomes, which play a central role in cytokine release and cell death. In this review we highlight recent advances in inflammasome research and propose key roles for inflammasome components in the progression of stroke damage.
引用
收藏
页码:205 / 212
页数:8
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