This study integrates complementary disease models to elucidate the role of CF modification in IPF: in vitro, BLM-stimulated MLE12 cells are used to simulate epithelial damage in the early stages of IPF, focusing on the regulation of alveolar epithelial autophagy and fibrosis by miR-15a-5p and CF modification; in vivo, a 21-day mouse model induced by BLM is used to reproduce the late-stage fibrosis phenotype, to assess the improvement of collagen deposition and lung function by inhibiting CF modification and regulating IGF1R. The gene discussed is IGF1R; the disease is idiopathic pulmonary fibrosis.