NLRP3炎症小体通路在矽肺纤维化中的作用及其作为治疗靶点的展望
The role of NLRP3 inflammasome pathway in silicosis-induced pulmonary fibrosis and its prospect as a therapeutic target
史梦雅 1刘保岩 1贺今1
作者信息
- 1. 山东第一医科大学(山东省医学科学院)山东省职业卫生与职业病防治研究院,济南 250062
- 折叠
摘要
吸入晶体二氧化硅颗粒可诱导矽肺,矽肺的发生与肺部炎症和肺纤维化的发生发展密切相关.NLRP3炎症小体已被确立为一种主要的促炎受体,用于感知环境危险信号.肺巨噬细胞吞噬二氧化硅颗粒后活化NLRP3炎症小体可能是诱导肺部氧化应激和持续炎症反应的重要机制.本文总结了NLRP3炎症小体通路在矽肺炎性反应和肺纤维化中的作用,并对其作为矽肺治疗的潜在靶点进行分析.
Abstract
Inhalation of crystalline silicon dioxide particles can induce silicosis,and the development of silicosis is closely related to the occurrence and development of pulmonary inflammation and pulmonary fibrosis.NOD-like receptor thermal protein domain associated protein 3(NLRP3)inflammasome has been established as a major proinflammatory receptor for sensing environmental danger signals.Activation of NLRP3 inflammasomes after phagocytosis of silicon dioxide particles by pulmonary macrophages may be an important mechanism to induce oxidative stress and sustained inflammatory response in the lung.This article summarizes the role of NLRP3 inflammasome in the inflammatory response and pulmonary fibrosis in silicosis,and analyzes it as a potential target for silicosis treatment.
关键词
二氧化硅/NLRP3炎症小体/信号通路/矽肺/治疗靶点/肺纤维化Key words
Silicon dioxide/NLRP3 inflammasome/Signaling pathway/Silicosis/Therapeutic target/Pulmonary fibrosis引用本文复制引用
基金项目
山东省自然科学基金(ZR2021MH178)
山东省中医药科技项目(2021Q082)
出版年
2024
NETL
NSTL
万方数据