细胞焦亡在急性呼吸窘迫综合征中的研究进展

Research progress of pyroptosis in acute respiratory distress syndrome

急性呼吸窘迫综合征(ARDS)的主要病理生理改变为肺血管内皮屏障被大量破坏、肺水肿、炎性细胞浸润等,严重者可发生难治性低氧血症。细胞焦亡是由天冬氨酸特异性半胱氨酸蛋白酶(caspase)触发、经一类保守的蛋白家族成员Gasdermin D(GSDMD)蛋白介导的细胞程序性坏死,表现为细胞不断胀大直至细胞膜破裂,导致细胞内容物释放进而激活强烈的炎症反应。焦亡在脓毒症导致的ARDS中发挥关键作用。本文主要对细胞焦亡的分子机制以及焦亡与ARDS关系的相关研究进行综述。

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.