Studies have indicated that the mechanism of IPF primarily involved defective PINK1/Parkin-mediated mitophagy in AEC, leading to increased occurrence of mtDNA damage, apoptosis, and senescence; these abnormalities collectively led to increased susceptibility to pulmonary fibrosis (Kim et al., 2020; Xiao et al., 2022). Here, PRKN is linked to idiopathic pulmonary fibrosis.