Consistently, in this study, we not only found excessive accumulation of 4-NHE, MDA, and ox-LDL in pulmonary fibrosis in vitro and in vivo, accompanied with the elevated expression of profibrotic proteins, including TGF-β, α-SMA, and Collagen I, but also demonstrated that strengthening of APN/CPT1A signaling was beneficial to restore the balance of lipid peroxides and profibrotic proteins, so as to suppress oxidative stress and alleviate pulmonary fibrosis. Here, TGFB1 is linked to pulmonary fibrosis.