活性氧激活TGF-β1通路调控哮喘气道上皮间质转分化的机制

Mechanism of ROS activate TGF-β1 pathway to regulate airway epithelial mesenchymal transition in asthma

支气管哮喘是一种常见的慢性呼吸系统疾病,其发病机制复杂,目前尚未完全清楚。近年来研究发现,氧化应激在支气管哮喘的发生发展中具有重要作用。当哮喘气道发生氧化应激损伤时,气道上皮细胞通过释放大量活性氧从而激活转化生长因子-β1(transforming growth factor-beta 1,TGF-β1)介导的多条信号通路,进而诱导上皮细胞发生间质转分化,参与哮喘气道重塑。该文对氧化应激调控TGF-β1诱导哮喘气道上皮细胞发生间质转分化的机制进行综述,旨为探讨哮喘气道发生重塑寻求新的理论基础,为哮喘气道重塑的治疗提供理论依据。

Bronchial asthma is a common chronic respiratory disease.Its pathogenesis is complex and still unclear.Recent studies have found that oxidative stress plays an important role in the development of bronchial asthma.When oxidative stress injury occurs in asthma airway,epithelial cells release a large amount of reactive oxygen species(ROS)to activate multiple signaling pathways mediated by transforming growth factor-beta 1(TGF-β1),and then induce epithelial mesenchymal transition(EMT)to participate in airway remodeling.This article reviews the mechanism of ROS activate TGF-β1 to induce EMT in asthma,aiming to seek a new theoretical basis for airway remodeling in asthmatic airway,and to provide a theoretical basis for the treatment of airway remodeling in asthma.