Is erythroferrone finally the long sought-after systemic erythroid regulator of iron?

Figure 1 Hepcidin in the regulation of systemic iron homeostasis. Systemic iron (Fe) homeostasis is primarily regulated by the hepcidin-ferroportin (FPN1) axis. Duodenal enterocytes import dietary Fe from several sources including heme Fe and non-heme Fe, which typically must be reduced at the level of the apical membrane by chemical reductants such as ascorbate[26,27] or by plasma membrane oxidoreductases (e.g., Dcytb), The reduced Fe then enters a common intracellular pool of Fe. “Sensing” the level of transferrin (TF) saturation and levels of Fe stores under conditions of Fe overload, hepatocytes up-regulate the expression of hepcidin, which is then released into the plasma where it can then bind to ferroportin (FPN1), thereby triggering FPN1 internalization and proteosomal degradation[1].