Airway remodeling and epithelial-mesenchymal transition markers

Airway remodeling refers to the persistent structural changes in the bronchial wall—such as subepithelial fibrosis, smooth muscle hypertrophy, and goblet cell hyperplasia—that contribute to airflow obstruction in chronic respiratory diseases like asthma and COPD [1]. Epithelial-mesenchymal transition (EMT) is a fundamental process driving these changes, wherein airway epithelial cells lose their adhesive properties and transform into myofibroblasts, which excessively produce extracellular matrix (ECM) [2]. Markers of this transition, including the loss of E-cadherin and the gain of Vimentin or alpha-smooth muscle actin (α-SMA), are used as diagnostic and prognostic indicators of fibrotic progression [3]. Although not a single molecular target, the pathways regulating EMT and remodeling, particularly the TGF-beta/Smad and Wnt/beta-catenin pathways, are major areas of drug development [4]. Current therapeutic strategies involve multi-kinase inhibitors like nintedanib or anti-inflammatory agents like corticosteroids to mitigate these structural alterations and preserve lung function [5].

Other names

Airway structural changesEMT-related proteinsBronchial remodeling markersFibrotic markers

Inhibition of tyrosine kinases, suppression of TGF-beta signaling, and modulation of inflammatory cytokine production to prevent fibroblast activation and extracellular matrix deposition.