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Identification of erythroferrone as an erythroid regulator of iron metabolism.

  • Author(s): Kautz, Léon;
  • Jung, Grace;
  • Valore, Erika V;
  • Rivella, Stefano;
  • Nemeth, Elizabeta;
  • Ganz, Tomas
  • et al.

Published Web Location

https://doi.org/10.1038/ng.2996
Abstract

Recovery from blood loss requires a greatly enhanced supply of iron to support expanded erythropoiesis. After hemorrhage, suppression of the iron-regulatory hormone hepcidin allows increased iron absorption and mobilization from stores. We identified a new hormone, erythroferrone (ERFE), that mediates hepcidin suppression during stress erythropoiesis. ERFE is produced by erythroblasts in response to erythropoietin. ERFE-deficient mice fail to suppress hepcidin rapidly after hemorrhage and exhibit a delay in recovery from blood loss. ERFE expression is greatly increased in Hbb(th3/+) mice with thalassemia intermedia, where it contributes to the suppression of hepcidin and the systemic iron overload characteristic of this disease.

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