急性呼吸窘迫综合征(acuterespiratorydistresssyndrome,ARDS)是临床面临的普遍难题,也是基础研究的热点,但其发病机制至今仍未完全阐明。研究证实,肺血管内皮细胞损伤导致的肺水肿液生成增多和肺上皮细胞损伤导致的肺水清除障碍是引起ARDS低氧血症的重要原因之一。对此,本文主要综述了近几年文献报道与ARDS肺水肿液产生机制有关的信号通路及其靶点,以期为ARDS新药研发和救治提供理论支持。
Acute respiratory distress syndrome (ARDS) is a common clinical problem and a hotspot in basic research. However, the pathogenesis has not yet been fully elucidated. Studies have shown that the increase of pulmonary edema fluid caused by pulmonary vascular endothelial cell damage and the lung water removal disorder caused by pulmonary epithelial cell damage are two key mechanisms of ARDS hypoxemia. In this review, we summarized the signal pathways and molecular targets involved in the form of pulmonary edema in ARDS during recent years,which can provide some theoretical support to new drug research and development and the treatment of ARDS.