NLRP3炎性小体——急性肺损伤的发病核心

doi:10.3969/j.issn.1002-1949.2019.03.017

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摘要临床上多种疾病均可引起急性肺损伤(ALI)，目前尚无特效治疗手段阻断其病程进展。肺部过度炎症反应是ALI发生发展的重要机制。本文综述NLRP3炎性小体及其相关信号通路在ALI/急性呼吸窘迫综合征（ARDS）发病机制中的作用，以期为ALI/ARDS的治疗提供全新的靶点。

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	罗亚岚
	许才明
	李兆霞
	蒋柳
	陈海龙

关键词 ：急性呼吸窘迫综合征（ARDS）, 急性肺损伤(ALI), 炎性小体

基金资助:国家自然科学基金资助项目（81573751）

通讯作者: 陈海龙（1962-），男，博士生导师，主任医师，教授，E-mail：hailongchen2013@163.com。

作者简介: 罗亚岚（1994-），女，硕士研究生，E-mail:luoyalanxueshu@163.com。

引用本文:

罗亚岚，许才明，李兆霞，蒋柳，陈海龙. NLRP3炎性小体——急性肺损伤的发病核心[J]. 中国急救医学, 2019, 39(3): 285-289.
Luo Ya-lan, Xu Cai-ming, Li Zhao-xia, Jiang Liu, Chen Hai-long. NLRP3 inflamasome—the core of acute lung injury. Chinese Journal of Critical Care Medicine, 2019, 39(3): 285-289.

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http://www.cnemergency.org.cn/CN/10.3969/j.issn.1002-1949.2019.03.017 或 http://www.cnemergency.org.cn/CN/Y2019/V39/I3/285

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