Wang Lei, Zhang Lipeng
Graduate School of Inner Mongolia Medical University, Hohhot 010000, Inner Mongolia Autonomous Region, China.
Department of Critical Care Medicine, the Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010000, Inner Mongolia Autonomous Region, China. Corresponding author: Zhang Lipeng, Email:
Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2021 Feb;33(2):249-251. doi: 10.3760/cma.j.cn121430-20200212-00179.
The main pathophysiological changes of acute respiratory distress syndrome (ARDS) are massive destruction of pulmonary vascular endothelial barrier, pulmonary edema, infiltration of inflammatory cells, and refractory hypoxemia in severe cases. Pyroptosis is programmed cell necrosis, triggered by caspase and mediated by proteins in a member of conserved protein family Gasdermin D (GSDMD), which manifests as continuous cell expansion until cell membrane rupture, leading to release of cell contents and activation of a strong inflammatory response. Pyroptosis plays a key role in the development of septic ARDS. In this paper, the molecular mechanism of pyroptosis and the related researches on pyroptosis and ARDS are reviewed.
急性呼吸窘迫综合征（ARDS）的主要病理生理变化为肺血管内皮屏障的大量破坏、肺水肿、炎症细胞浸润，严重时出现难治性低氧血症。细胞焦亡是一种程序性细胞坏死，由半胱天冬酶触发，并由保守蛋白家族Gasdermin D（GSDMD）成员中的蛋白质介导，其表现为细胞持续扩张直至细胞膜破裂，导致细胞内容物释放并激活强烈的炎症反应。细胞焦亡在脓毒症性ARDS的发生发展中起关键作用。本文就细胞焦亡的分子机制以及细胞焦亡与ARDS的相关研究进行综述。
