Airway remodeling refers to persistent structural changes in the airway wall that occur as a consequence of chronic inflammation and repeated injury-repair cycles. In asthma, remodeling includes subepithelial fibrosis (collagen deposition beneath the basement membrane), smooth muscle hypertrophy and hyperplasia (up to 3-fold increase in muscle mass), goblet cell metaplasia (mucous gland hyperplasia causing excess mucus production), angiogenesis (new vessel formation in the airway wall), and epithelial desquamation. These structural changes contribute to fixed airway obstruction, airway hyperresponsiveness, and progressive loss of lung function even between exacerbations. TH2 cytokines (IL-4, IL-5, IL-13), eosinophilic inflammation, and transforming growth factor-beta (TGF-β) drive remodeling. In COPD, remodeling manifests differently: small airway fibrosis and narrowing, emphysematous destruction of alveolar walls (protease-antiprotease imbalance with neutrophil elastase and matrix metalloproteinases degrading elastin), mucous gland hypertrophy in large airways (Reid index >0.5), and loss of elastic recoil causing expiratory airflow limitation and air trapping. Alpha-1 antitrypsin deficiency accelerates emphysematous destruction through uninhibited neutrophil elastase activity. Inhaled corticosteroids partially suppress inflammatory-mediated remodeling in asthma but have limited impact on established structural changes; early and sustained anti-inflammatory therapy is...