Porcine epidemic diarrhea virus (PEDV) infection leads to immunosuppression and clinical symptoms in piglets, including vomiting, watery diarrhea, dehydration, and even death. Mitophagy sustains mitochondrial energy homeostasis and quality through the removal of damaged mitochondria. However, PEDV disrupts mitochondrial homeostasis, which affects cellular energy supply and reproduction. Despite existing research, the mechanisms underlying PEDV pathogenesis and its interaction with the innate immune system remain largely unclear. Therefore, we aimed to clarify the mechanism of PEDV-induced mitophagy and its relationship with apoptosis and Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway after PEDV infection. We infected Vero and IPEC-J2 cells with PEDV. Then, we evaluated mitochondrial morphology, structural proteins of PEDV, reactive oxygen species (ROS) levels, and mitochondrial membrane potential using transmission electron microscopy, confocal laser scanning microscopy, and flow cytometry. We identified mitophagy-related proteins through immunoprecipitation and western blotting. We examined the effects of mitophagy on PEDV proliferation and JAK1-STAT1 signaling via western blotting and indirect immunofluorescence. PEDV infection led to mitochondrial damage and the production of mitophagosome-like vesicles. Subsequently, the PEDV structural N protein initiated mitophagy through ubiquitinating mitofusin 2 (MNF2) via the PINK1/Parkin pathway. Moreover, mitophagy promoted PEDV replication. In the early stage of PEDV infection, PEDV infection inhibits apoptosis by promoting mitophagy. PEDV infection significantly decreased the expression of JAK1, STAT1, interferon regulatory factor 9, and phosphorylated STAT1, inhibiting nuclear translocation and promoting replication. Overall, PINK1/Parkin-mediated mitophagy regulated PEDV-induced apoptosis and JAK/STAT1 expression. These findings provide a scientific basis for elucidating the pathogenic and immune escape mechanisms of PEDV.