细胞焦亡及其在心肌缺血再灌注损伤中作用机制

黄兰松, 刘燕, 黄照河. 细胞焦亡及其在心肌缺血再灌注损伤中作用机制[J]. 临床心血管病杂志, 2021, 37(2): 182-186. doi: 10.13201/j.issn.1001-1439.2021.02.019
引用本文: 黄兰松, 刘燕, 黄照河. 细胞焦亡及其在心肌缺血再灌注损伤中作用机制[J]. 临床心血管病杂志, 2021, 37(2): 182-186. doi: 10.13201/j.issn.1001-1439.2021.02.019
HUANG Lansong, LIU Yan, HUANG Zhaohe. Pyroptosis and its role in myocardial ischemia reperfusion injury[J]. J Clin Cardiol, 2021, 37(2): 182-186. doi: 10.13201/j.issn.1001-1439.2021.02.019
Citation: HUANG Lansong, LIU Yan, HUANG Zhaohe. Pyroptosis and its role in myocardial ischemia reperfusion injury[J]. J Clin Cardiol, 2021, 37(2): 182-186. doi: 10.13201/j.issn.1001-1439.2021.02.019

细胞焦亡及其在心肌缺血再灌注损伤中作用机制

  • 基金项目:

    国家自然科学基金项目(No:81860797)

详细信息
    通讯作者: 黄照河,E-mail:bshuangzhaohe@163.com
  • 中图分类号: R542.2

Pyroptosis and its role in myocardial ischemia reperfusion injury

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  • 急性心肌梗死是世界范围内发病率和病死率的主要原因,缺血心肌血流恢复可改善心肌功能,然而血流再通可能会导致严重心肌损伤,即心肌缺血再灌注损伤(MIRI)。细胞焦亡是一种高度促炎的细胞程序性死亡。活化的半胱天冬氨酸蛋白酶(caspases)裂解造孔蛋白Gasdermin D(GSDMD)引起质膜破裂,导致促炎因子白细胞介素(IL)-1β和IL-18释放。研究表明,细胞焦亡参与MIRI发生发展。本文主要对细胞焦亡及其在MIRI中作用机制作一综述,以期为MIRI诊疗提供理论依据和现实可行性。
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收稿日期:  2020-07-09

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