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Significance Iron regulatory proteins (IRPs) control cellular iron homeostasis.Irp2 knockout mice show symptoms of neurological disorders, which are considered to result from impaired mitochondrial activity. To explore the involvement of Irp2 in mitochondrial function, we examined the metabolic pathways of Irp2-depleted mouse embryonic fibroblasts. We found that Irp2 deficiency switches cellular metabolic pathways from oxidative phosphorylation (OXPHOS) to aerobic glycolysis. We further revealed that Irp2 deficiency induces the expression of Hif1α and Hif2α; Hif1α enhances aerobic glycolysis by upregulating its target genes related to the glycolytic pathway, and Hif2α suppresses mitochondrial Fe–S biosynthesis and OXPHOS. This identified mechanism implies that high-energy-need tissues, such as the central nervous system, could be affected when Irp2 is deficient, leading to neurological disorders.

Iron regulatory protein 2 modulates the switch from aerobic glycolysis to oxidative phosphorylation in mouse embryonic fibroblasts