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Figure 3 4 Pathological links between EMT and pulmonary fibrosis EMT plays a central regulatory role in pulmonary fibrosis, characterized by remodeling of alveolar-epithelial phenotypes, down-regulation of epithelial markers (e.g., E-cadherin) and up-regulation of mesenchymal markers (e.g., vimentin, N-cadherin), together with fibroblast-to-myofibroblast differentiation that establishes a pro-fibrotic micro-environment and drives disease progression ( In pneumoconiosis (e.g., silicosis), AT2 cells similarly undergo EMT but with distinct upstream triggers