摘要
急性肺损伤/急性呼吸窘迫综合征（ALI/ARDS）是由于弥漫性肺泡-毛细血管膜损伤导致的以非心源性肺水肿和炎症为病理特征的急性呼吸衰竭,ARDS是ALI的严重阶段,临床上致死率高.炎症反应、细胞凋亡等在ALI的发生和发展过程中产生了重要的作用,介导这一系列病理反应过程的信号通路已成为研究的热点.近年来,相关研究表明,p38丝裂原活化蛋白激酶（p38MAPK）在参与ALI炎症反应和细胞凋亡中发挥了重要的作用,有可能成为治疗ALI的新靶点.
Acute lung injury （ALI） and acute respiratory distress syndrome （ARDS） are acute respiratory failure due to acute diffuse damage to the membrane of alveolar and capillary, having the pathological features of the noncardiac pulmonary edema and inflammation. ARDS with a very high fatality rate is a serious stage of ALI. Inflammation, cell apoptosis and so on, play important roles in the development of ALI. Cell signaling pathways mediating these pathological reaction processes have become the focus of research. Recent studies have shown that p38 mitogen - activated protein kinase （p38MAPK） plays a very important role in the inflammation and the cell apoptosis of ALI. It may become a new target of the treatment of lung injury.
出处
《中国急救医学》
CAS
CSCD
北大核心
2013年第11期1045-1048,共4页
Chinese Journal of Critical Care Medicine
基金
南京军区122工程重点培养对象资助项目（JQZD200905）
南京军区青年基金课题（2011030）
