细胞焦亡与脑卒中

Pyroptosis and stroke

细胞焦亡是一种依赖于caspase-1和caspase-4/5/11的程序性细胞死亡方式,参与感染性疾病和神经系统疾病等的发展过程。细胞焦亡主要由经典炎症小体途径和非经典炎症小体途径介导,而经典炎症小体途径在脑卒中中活化并且加重脑损伤,抑制炎症小体和下游分子能减轻损伤发挥保护作用。经典炎症小体途径介导了脑卒中损伤,因而焦亡成为脑卒中干预的潜在靶点。本文就细胞焦亡与脑卒中关系的研究进展进行综述,旨在为相关领域的研究提供参考。

Pyroptosis is a form of inflammatory programmed cell death activated by caspase-1 and caspase-4/5/11, and involves in the pathogenesis of infectious diseases and nervous system diseases. Pyroptosis is mediated by canonical inflammasome pathway and non-canonical inftammasome pathway. The canonical inflammasome pathway is activated in stroke and aggravates brain injury. Inhibition of inflammasome, caspase-1, IL-1 and IL-18 ameliorates brain injury. These studies indicate that canonical inflammasome pathway contributes to post-stroke brain injury, therefore, pyroptosis has become a potential therapeutic target for preventing excessive cell death during stroke. We reviewed the relationship between pyroptosis and stroke to provide some perspectives on future researches in this field.