An IDH1-vitamin C crosstalk drives human erythroid development by inhibiting pro-oxidant mitochondrial metabolism

Abstract

Gonzalez-Menendez et al. show that terminal erythroid differentiation is dependent on the suppression of mitochondrial metabolism. Disturbances in levels of the α-ketoglutarate and IDH1 TCA-cycle regulators result in ineffective erythropoiesis, with generation of morphologically abnormal erythroblasts. Vitamin C restores redox homeostasis and rescues late-stage erythropoiesis by scavenging reactive oxygen species.