Effects of mitophagy activation on ferroptosis and meat quality during postmortem storage of Esox lucius

Previous studies have established that ferroptosis substantially affects muscle quality. Although mitophagy is a recognized regulator of ferroptosis, its specific role in postmortem muscle ferroptosis and meat quality development remains unclear. In this study, mitophagy activity was modulated in the dorsal muscle of Esox lucius through treatment with Mdivi-1 or normal saline, aiming to elucidate the mechanism by which mitophagy induces ferroptosis during postmortem storage. The results indicated that Mdivi-1 treatment downregulated the expression of key mitophagy-related proteins (Parkin and BNIP3) and attenuated the loss of mitochondrial membrane potential. This suppression subsequently reduced mitochondrial ferrous ion release, alleviated the impairment of the GSH/GPX4 antioxidant system, decreased lipid peroxidation, and ultimately delayed the ferroptosis process in postmortem muscle cells. Importantly, inhibition of the mitophagy-mediated ferroptosis pathway effectively mitigated myofibrillar structural disintegration and the reduction in shear force. These findings enhance the understanding of ferroptosis mechanisms in postmortem muscle and suggest potential strategies for improving fish meat quality. • Mitophagy is activated in postmortem fish muscle and inhibited by Mdivi-1. • Mitophagy induces ferroptosis by promoting ferrous ion release and GPX4 degradation. • Mitophagy-mediated ferroptosis affects postmortem fish meat tenderness.