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上皮间质转化与重度哮喘糖皮质激素抵抗的关系研究进展
引用本文:张仕清.上皮间质转化与重度哮喘糖皮质激素抵抗的关系研究进展[J].大连医科大学学报,2022,44(2):163-168.
作者姓名:张仕清
作者单位:大连医科大学 研究生院,辽宁 大连 116044
基金项目:江苏省“333工程”科研项目(BRA2020015)
摘    要:上皮间质转化(epithelial-mesenchymal transition,EMT)即上皮细胞失去其功能及特性转化为间质细胞的表型,目前的大部分研究已经证实了EMT在支气管哮喘(哮喘)气道重塑和气道纤维化发展过程中的重要作用。气道炎症、气道高反应性和气道重塑是支气管哮喘的主要病理生理学特征。目前糖皮质激素(glucocorticoid,GC)是临床控制哮喘急性发作及延缓哮喘恶化的一线药物。但是仍有一部分哮喘患者即使是使用大剂量的GC,仍然不能控制哮喘发作。这部分哮喘患者几乎全部已经进展至重度哮喘阶段,其小气道的结构和功能不可逆转。本综述旨在以EMT作为切入点讨论EMT在重度哮喘GC抵抗诊断和治疗中的潜在价值。

关 键 词:上皮间质转化  重度哮喘  糖皮质激素  气道重塑  组蛋白去乙酰化酶2
收稿时间:2021/4/20 0:00:00
修稿时间:2022/3/9 0:00:00

Research progress on the relationship between epithelial-mesenchymal transition and glucocorticoid resistance in severe asthma
ZHANG Shiqing.Research progress on the relationship between epithelial-mesenchymal transition and glucocorticoid resistance in severe asthma[J].Journal of Dalian Medical University,2022,44(2):163-168.
Authors:ZHANG Shiqing
Abstract:Epithelial-mesenchymal transition (EMT) is the phenotype of epithelial cells that lose their functions and characteristics and transform into mesenchymal cells. Most of current studies have confirmed the important role of EMT in the development of airway remodeling and airway fibrosis in bronchial asthma (asthma). Airway inflammation, airway hyperresponsiveness and airway remodeling are the main pathophysiological characteristics of bronchial asthma. At present, glucocorticoids are the first-line control drugs for clinical control of acute asthma attacks and alleviation of asthma exacerbations. However, there are still some asthma patients who use high-dose of glucocorticoids and can''t control asthma attacks. Almost all of these asthma patients progress to severe asthma stage with irreversible damages to the small airway structure and function. This review aims to use EMT as an entry point to discuss the potential roles of EMT in the occurrence and treatment of glucocorticoid resistance in severe asthma.
Keywords:epithelial-mesenchymal transition (EMT)  severe asthma  glucocorticoid  airway remodeling  histone deacetylase 2
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