Interleukin-1 and brain inflammation

被引：38

作者：

Brough, David ^{[1
]}

Denes, Adam ^{[1
,2
]}

机构：

[1] Univ Manchester, Fac Life Sci, Manchester M13 9PT, Lancs, England

[2] Hungarian Acad Sci, Inst Expt Med, Lab Mol Neuroendocrinol, Budapest, Hungary

来源：

IUBMB LIFE | 2015年 / 67卷 / 05期

关键词：

Ca2+ signalling; cell death; human molecular disease; PROGRAMMED NECROSIS; RECEPTOR ANTAGONIST; CELL-DEATH; SYSTEMIC INFLAMMATION; CEREBRAL-ISCHEMIA; INDUCED RELEASE; IL-1; FAMILY; IL-1-ALPHA; IL-1-BETA; DAMAGE;

D O I：

10.1002/iub.1377

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Acute brain injuries such as caused by stroke are amongst the leading causes of death and are the leading cause of disability. Despite this there are very limited therapeutic options, and new therapeutic strategies and targets are required. Inflammation is known to exacerbate brain injury and is now considered as a potential therapeutic target. The damaging inflammation that occurs after acute brain injury is driven by pro-inflammatory members of the interleukin (IL)-1 cytokine family, namely, IL-1 and IL-1. Previous research efforts have focussed on the biology and contribution of IL-1. However, we now recognise that IL-1 is an early and important mediator of inflammation after injury. This review focuses on what is known about IL-1, its regulation and its contribution to brain injury. Inhibiting mechanisms regulating the processing and release of IL-1 may offer new therapeutic targets for the treatment of devastating acute brain injuries. (c) 2015 IUBMB Life, 2015 67(5):323-330, 2015

引用

页码：323 / 330

页数：8

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