In this study, we not only demonstrated that inhibition of PINK1/Parkin/mitophagy partly weakened the protective effect of OGG1 inhibition against BLM-induced pulmonary fibrosis in vivo, but also disclosed that PINK1 overexpression effectively attenuated M2 macrophages-mediated oxidative stress, mitochondrial dysfunction in fibroblasts in vitro. This evidence concerns the gene PRKN and pulmonary fibrosis.