Erythroid FGF23 Directly Inhibits Red Cell Production in Mouse Models

Fibroblast growth factor 23 (FGF23) is a bone-derived hormone that regulates systemic phosphate homeostasis and vitamin D metabolism [1, 2]. In clinical practice, elevated circulating levels of this hormone are frequently observed in patients with iron deficiency anemia and chronic kidney disease, where they correlate with adverse cardiovascular outcomes and renal disease progression [3, 4]. While oral iron supplementation can effectively lower hormone concentrations, certain intravenous iron formulations paradoxically trigger a surge in the intact, biologically active form of the protein, often leading to renal phosphate wasting and symptomatic hypophosphatemia [5, 6]. This complex relationship suggests that the hormone may exert physiological effects beyond mineral regulation, particularly within the hematopoietic compartment [7]. A new study now clarifies the specific cellular source and local mechanism by which this factor directly impairs red blood cell maturation.