IDENTIFICATION OF ERYTHROFERRONE AS AN ERYTHROID REGULATOR OF IRON METABOLISM

By Léon Kautz, Grace Jung, E. Valore, S. Rivella, E. Nemeth, T. Ganz. Nature Genetics, 2014

1,056 citations recorded by the source corpus.

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 Hbbth3/+ mice with thalassemia intermedia, where it contributes to the suppression of hepcidin and the systemic iron overload characteristic of this disease.

Subfields: Genetics, Hematology, Physiology

View Paper: https://www.semanticscholar.org/paper/bd927d14b4b09c82dd9d1af256788927fecb9d4a

Citations in the corpus

• Iron metabolism and iron disorders revisited in the hepcidin era (2020, neutral): “52 In hypoxia hepcidin is also suppressed in vitro by soluble hemojuvelin, released by furin, 53 an effect unclear in vivo , and by platelet-derived growth factor-BB in volunteers exposed to hypoxia.”