Brough David, Denes Adam
Faculty of Life Sciences, University of Manchester, Manchester, UK.
Laboratory of Molecular Neuroendocrinology, Institute of Experimental Medicine, Budapest, Hungary.
IUBMB Life. 2015 May;67(5):323-30. doi: 10.1002/iub.1377. Epub 2015 Apr 23.
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-1α and IL-1β. Previous research efforts have focussed on the biology and contribution of IL-1β. However, we now recognise that IL-1α is an early and important mediator of inflammation after injury. This review focuses on what is known about IL-1α, its regulation and its contribution to brain injury. Inhibiting mechanisms regulating the processing and release of IL-1α may offer new therapeutic targets for the treatment of devastating acute brain injuries.
诸如中风所导致的急性脑损伤是主要的死亡原因之一，也是导致残疾的首要原因。尽管如此，目前的治疗选择非常有限，因此需要新的治疗策略和靶点。众所周知，炎症会加剧脑损伤，现在炎症被视为一个潜在的治疗靶点。急性脑损伤后发生的有害炎症是由白细胞介素（IL）-1细胞因子家族的促炎成员，即IL-1α和IL-1β驱动的。以往的研究工作主要集中在IL-1β的生物学特性和作用上。然而，我们现在认识到IL-1α是损伤后炎症的早期重要介质。这篇综述聚焦于目前已知的关于IL-1α的信息、其调节机制及其对脑损伤的作用。抑制调节IL-1α加工和释放的机制可能为治疗严重急性脑损伤提供新的治疗靶点。
