Specifically, TGF-β1/Smad signaling significantly contributes to IPF pathogenesis by facilitating the activation, proliferation, and differentiation of epithelial cells and collagen-producing myofibroblasts, ultimately exacerbating ECM deposition and fibrosis development (Wu et al., 2021; Peng et al., 2022). Here, TGFB1 is linked to idiopathic pulmonary fibrosis.