p38信号通路在呼吸机相关性肺损伤中的作用  

p38MAPK signaling pathway is involved in ventilator-induced lung injury

作　　者：李从烨 高成金[1,2] 张翔宇[1,2] 

机构地区：[1]同济大学附属第十人民医院急诊医学科,上海200072 [2]同济大学附属第十人民医院重症医学科,上海200072

出　　处：《同济大学学报（医学版）》2014年第4期126-128,132,共4页Journal of Tongji University(Medical Science)

基　　金：国家自然科学基金(81000024)

摘　　要：呼吸机相关性肺损伤(ventilator-induced lung injury,VILI)是由机械通气产生的严重并发症,VILI的类型主要包括:气压伤(baratrauma)、容积伤(volutrauma)、肺萎陷伤(atelectrauma)、生物伤(biotrauma),目前临床上仍无有效的治疗策略。丝裂原活化蛋白激酶家族可以在一系列细胞外刺激下参与细胞应答,在哺乳动物中,已经发现了ERKs(extracellular signal-regulated kinase)、JNK/SAPK(c-jun N-terminal/stress-activated protein kinase)、ERK5/BMK1(ERK/big MAP kinase 1)以及p38四个亚家族。随着对VILI的不断深入研究,p38通路被认为参与了VILI的发生机制,深入研究p38信号通路在VILI中的作用,可为临床提供新的治疗靶点。Ventilator-induced lung injury （VILI） is one of the most serious complications of mechanical ventilation. There are four types of VILI, namely baratrauma, volutrauma, ateletrauma and biotrauma. Members of mitogen-activated protein kinase family participate in cellular responses to a wide range of extracellular stimuli. Four subfamilies of MAPkinase, ERK, JNK/SAPK, ERK5/ BMKI and p38 have been identified in mammalian cells. The p38 MAPK （mitogen-activated protein kinase） signaling pathway is considered one of the mechanisms of VILI. In this article we review the involvement of p38 MAPK in VILI, which may provide a novel target for prevention and treatment of VILI.

关 键 词：p38M APK 信号通路 呼吸机相关性肺损伤 

分 类 号：R563.8[医药卫生—呼吸系统]