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- W2006046265 abstract "Tomas Ganz and colleagues identify a new regulator of iron metabolism, erythroferrone, that is produced by erythroblasts in response to erythropoietin and suppresses hepcidin expression during stress erythropoiesis. They further show that erythroferrone levels are highly elevated in a mouse model of β-thalassemia, contributing to hepcidin suppression and iron overload in this model. 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." @default.
- W2006046265 created "2016-06-24" @default.
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- W2006046265 date "2014-06-01" @default.
- W2006046265 modified "2023-10-17" @default.
- W2006046265 title "Identification of erythroferrone as an erythroid regulator of iron metabolism" @default.
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- W2006046265 doi "https://doi.org/10.1038/ng.2996" @default.
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