Airway remodeling

Airway remodeling, also known as airway structural alterations, encompasses the complex and heterogeneous architectural changes in the bronchial wall resulting from chronic inflammation and repetitive injury-repair cycles [1, 10, 20]. This pathological process is characterized by epithelial denudation, goblet cell hyperplasia, subepithelial fibrosis (thickening of the reticular basement membrane), increased airway smooth muscle mass through both hyperplasia and hypertrophy, and enhanced vascularization [2, 11, 23]. These alterations lead to progressive and often irreversible narrowing of the airway lumen, which contributes to fixed airflow obstruction and bronchial hyperresponsiveness in chronic respiratory diseases such as asthma and COPD [4, 8, 9]. While traditional therapies like inhaled corticosteroids primarily address the underlying inflammatory environment, they often exhibit limited efficacy in reversing established structural modifications once they have occurred [11, 12, 18]. Emerging biological therapies targeting specific inflammatory drivers, such as IL-5 (mepolizumab), IL-4/IL-13 (dupilumab), and TSLP (tezepelumab), are currently being evaluated for their potential to mitigate or prevent these remodeling processes, which remain a significant cause of long-term lung function decline [5, 12, 16, 17].

Other names

Airway remodelingBronchial remodelingSubepithelial fibrosisAirway wall thickeningChronic airway structural changes

Reduction of airway inflammation, inhibition of Th2 cytokine signaling (IL-4, IL-5, IL-13), suppression of epithelial-derived alarmins (TSLP), and relaxation of airway smooth muscle to mitigate mechanical strain.