ACTA1 and pulmonary fibrosis: In cigarette-smoke extract (CSE)-induced in-vitro models, airway epithelial cells undergoing CSE-driven EMT and TGF-β1/SMAD3 activation lose epithelial markers (E-cadherin), gain mesenchymal traits (up-regulation of N-cadherin, Slug, α-SMA), exhibit greater motility and ECM synthesis, and markedly elevate fibrotic proteins such as collagen IV and fibronectin-1, thereby further promoting lung fibrosis (86).