焦亡在ARDS引起的肺血管内皮细胞功能障碍中的作用  

The Role of Pyroptosis in the Dysfunction of Pulmonary Endothelial Cells Caused by ARDS

作　　者：田雨[1] 詹柱 张安[1] 

机构地区：[1]重庆医科大学附属第二医院重症医学科,重庆 [2]重庆医科大学附属第二医院感染科,重庆

出　　处：《临床医学进展》2024年第3期1895-1900,共6页Advances in Clinical Medicine

摘　　要：急性呼吸窘迫综合征(Acute Respiratory Distress Syndrome, ARDS)是一种严重且难以控制的急性肺部炎症情况,常与多种损伤因素相关。细胞焦亡是一种由炎性半胱氨酸蛋白酶(caspase)触发的程序性细胞死亡方式,其在ARDS的发生发展过程中发挥着重要作用。本文将综述肺血管内皮细胞焦亡在ARDS进展中的作用,并指出其作为潜在药物靶点的重要意义。Acute Respiratory Distress Syndrome (ARDS) is a severe and challenging acute lung inflammation condition often associated with various injurious factors. Pyroptosis is a form of programmed cell death triggered by inflammatory caspases. It plays a significant role in the occurrence and progression of ARDS. This article will review the role of pulmonary vascular endothelial cell pyroptosis in the advancement of ARDS and underscore its importance as a potential drug target.

关 键 词：急性呼吸窘迫综合征 肺血管内皮细胞 焦亡 信号通路 治疗 

分 类 号：R56[医药卫生—呼吸系统]