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Cover Credit: Schematic illustration of the potential mechanisms underlying mitophagy against hypoxia-ischemia-induced neuronal ferroptosis. In neonatal rat HIBD, mitophagy is activated as a protective response to maintain mitochondrial homeostasis and energy metabolism. BNIP3-dependent mitophagy mediated by Tat-SPK2 peptide maintains iron and redox homeostasis by facilitating P62-KEAP1-NRF2 pathway, thereby ameliorating lipid peroxidation and neuronal ferroptosis. (DOI 10.1038/s41401-024-01365-x). See the article in pages 33–51