Abstract: The frequent outbreaks of avian influenza have caused huge economic losses to the poultry industry. Its pathogen, avian influenza virus (AIV), can infect not only birds; some subtypes can also cross species barriers and infect humans and other animals, posing a continuous threat to global biosafety. Autophagy, as a highly conserved degradation process that maintains cellular homeostasis, plays a dual role (both antiviral and proviral) in viral infections. Research has shown that AIV can actively intervene in autophagic flux through viral proteins such as NS1, M2, and PB1-F2 to obtain the membrane structures required for self-replication and to evade host immune monitoring, especially targeting mitophagy processes. In addition, virus-induced mitochondrial dysfunction not only leads to an outbreak of reactive oxygen species, but in severe cases, it can further cause mitochondrial oxidative membrane rupture and death, known as “mitoxyperilysis”. Therefore, this article systematically reviews the signaling network of AIV-activated mitophagy, focusing on the interaction between viral proteins and core autophagy components, and deeply explores the oxidative stress, lipid peroxidation, and “mitoxyperilysis” effects caused by mitophagy dysfunction, aiming to provide a theoretical basis for the development of new antiviral strategies targeting host mitochondrial homeostasis.