Taken together, our findings highlight the critical role of TRPA1 channels in the pathogenesis of IPF by promoting the phosphorylation of TGF-β1-Smad2 signaling and regulating the polarization of macrophages to the M2 phenotype, which further promotes tissue repair and collagen deposition. Here, TGFB1 is linked to idiopathic pulmonary fibrosis.