{"title":"Mechanisms of airway remodeling in asthma","authors":"James G. Martin, Neil Verma","doi":"10.1016/j.ddmec.2012.11.004","DOIUrl":null,"url":null,"abstract":"<div><p><span><span>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 </span>pharmacological therapies target </span>goblet cell<span> differentiation. Airway smooth muscle hyperplastic growth is mediated via the epidermal growth factor receptor<span><span> 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<span> may reduce airway matrix protein deposition. Studies of </span></span>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.</span></span></p></div>","PeriodicalId":72843,"journal":{"name":"Drug discovery today. Disease mechanisms","volume":"9 3","pages":"Pages e95-e102"},"PeriodicalIF":0.0000,"publicationDate":"2012-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ddmec.2012.11.004","citationCount":"6","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Drug discovery today. Disease mechanisms","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1740676512000223","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 6
Abstract
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.