哮喘气道重塑的机制

James G. Martin, Neil Verma
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引用次数: 6

摘要

气道重塑是哮喘发病机制的重要组成部分。上皮介质可以驱动其他组织的变化,包括细胞外基质、气道平滑肌和支气管血管床。几种新的药物治疗针对杯状细胞分化。气道平滑肌增生性生长是通过表皮生长因子受体通过cysLT受体1介导的,但也对各种其他药物干预有反应。抗il -5治疗和前列腺素E受体激动剂可减少气道基质蛋白沉积。目前缺乏对血管重构的研究。有必要开发具有可接受的毒性并在人类受试者中得到验证的重塑抑制剂。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Mechanisms of airway remodeling in asthma

Airway remodeling is a crucial part of the pathogenesis of asthma. Epithelial-mediators may drive changes in other tissues, including the extracellular matrix, airway smooth muscle and the bronchial vascular bed. Several novel pharmacological therapies target goblet cell differentiation. Airway smooth muscle hyperplastic growth is mediated via the epidermal growth factor receptor via the cysLT receptor 1 but is also responsive to a variety of other pharmacological interventions. Anti-IL-5 treatment and prostaglandin E receptor agonists may reduce airway matrix protein deposition. Studies of vascular remodeling are lacking. There is a need for the development of inhibitors of remodeling that have acceptable toxicity and are validated in human subjects.

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