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Epithelial-mesenchymal transition in the pathophysiology of airway remodelling in asthma

机译:哮喘气道重塑的病理生理过程中上皮-间质转化

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摘要

Purpose of review: We currently understand little about the mechanisms that lead to airway remodeling in asthma. The origin of the mesenchymal cells that contribute to fibrosis of the airway is poorly understood. However, emerging evidence suggests that the airway epithelium could contribute to airway remodeling through the process of epithelial-mesenchymal transition (EMT) following environmental challenge. In this review, we will discuss the mechanistic features of EMT and highlight recent descriptions of EMT in the airway to further define the role of the airway epithelium in the pathogenesis of asthma. Recent findings: Growth factors, inflammatory mediators, and matricellular proteins expressed following exposure to environmental insults are known to induce downregulation of epithelial cell-cell adhesions and promote mesenchymal gene expression programs both in vitro and in vivo. These results demonstrate that the plastic and dynamic airway epithelium may contribute to airway remodeling via EMT in asthma. Summary: It is becoming increasingly clear that the airway epithelium orchestrates inflammatory and remodeling responses of the airway. Understanding the regulatory mechanisms involved in epithelial plasticity will be crucial to determine effective therapies to halt the progression of airway remodeling in asthma.
机译:审查目的:我们目前对导致哮喘气道重塑的机制了解甚少。导致气道纤维化的间充质细胞的起源知之甚少。然而,越来越多的证据表明,在环境挑战后,气道上皮可能通过上皮-间质转化(EMT)过程促进气道重塑。在这篇综述中,我们将讨论EMT的机制特征,并着重介绍EMT在气道中的最新描述,以进一步定义气道上皮在哮喘发病机理中的作用。最近的发现:暴露于环境损伤后表达的生长因子,炎性介质和基质细胞蛋白可诱导上皮细胞粘附的下调,并在体外和体内促进间充质基因表达程序。这些结果表明,可塑性和动态气道上皮可能通过哮喘中的EMT促进气道重塑。简介:越来越明显的是,气道上皮协调了气道的炎症反应和重塑反应。了解涉及上皮可塑性的调节机制对于确定有效的治疗方法以制止哮喘中气道重塑的进展至关重要。

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