Airway remodeling and Epithelial-Mesenchymal Transition (EMT) markers (EMT markers)

Airway remodeling refers to the structural alterations of the bronchial walls, including subepithelial fibrosis, smooth muscle hypertrophy, and goblet cell hyperplasia, which are hallmark features of chronic respiratory diseases like asthma and COPD (NIH, 2023). A central driver of this process is the epithelial-mesenchymal transition (EMT), a biological program where airway epithelial cells lose their polarity and cell-cell adhesion (marked by decreased E-cadherin) and acquire a mesenchymal phenotype (marked by increased vimentin and alpha-smooth muscle actin) (Frontiers in Immunology, 2020). This transition facilitates the accumulation of myofibroblasts and excessive extracellular matrix deposition, leading to irreversible airflow obstruction and persistent respiratory symptoms (NIH, 2025). While 'Airway remodeling/EMT markers' represents a descriptive category of biomarkers and a biological process rather than a single molecular target, these markers are critical for monitoring disease progression and evaluating the efficacy of anti-fibrotic and anti-inflammatory therapies (Canadian Respiratory Journal, 2023). Therapeutic strategies often focus on inhibiting upstream signaling pathways, such as TGF-beta or Th2 cytokines (IL-4/IL-13), to modulate these markers and mitigate structural damage (NIH, 2023).

Other names

Airway structural changesEpithelial-to-mesenchymal transition markersBronchial remodeling markersAirway fibrosis markers

Modulation of signaling pathways such as TGF-beta, IL-13, IL-4, and Wnt/beta-catenin to inhibit the phenotypic transition of epithelial cells into mesenchymal-like cells and reduce subepithelial fibrosis and extracellular matrix deposition (NIH, 2023; Canadian Respiratory Journal, 2023).