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. The gene discussed is ACTA1; the disease is pulmonary fibrosis.