Furthermore, the ASIC2 overexpression plasmid was used to rescue the protein levels of ASIC2 in A549 and AECs, which stimulated EMT and ECM accumulation and inhibited apoptosis and autophagy when compared with the TGF-β1 + PTE group, suggesting that PTE inhibited pulmonary fibrosis by downregulating ASIC2. Here, ASIC2 is linked to pulmonary fibrosis.