In summary, the results of this study suggest that the collagen metabolism imbalance, inflammatory responses, and EMT activation are the core processes of IPF, and that the TGF-β1/Smad3 and Wnt/β-catenin signaling pathways and related signal transduction molecules are key targets for the treatment of IPF. Here, SMAD3 is linked to idiopathic pulmonary fibrosis.