Targeting the Hepcidin-Ferroportin Axis in the Diagnosis and Treatment of Anemias

The hepatic peptide hormone hepcidin regulates dietary iron absorption, plasma iron concentrations, and tissue iron distribution. Hepcidin acts by causing the degradation of its receptor, the cellular iron exporter ferroportin. The loss of ferroportin decreases iron flow into plasma from absorptive...

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Main Author: Elizabeta Nemeth
Format: Article
Language:English
Published: Wiley 2010-01-01
Series:Advances in Hematology
Online Access:http://dx.doi.org/10.1155/2010/750643
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author Elizabeta Nemeth
author_facet Elizabeta Nemeth
author_sort Elizabeta Nemeth
collection DOAJ
description The hepatic peptide hormone hepcidin regulates dietary iron absorption, plasma iron concentrations, and tissue iron distribution. Hepcidin acts by causing the degradation of its receptor, the cellular iron exporter ferroportin. The loss of ferroportin decreases iron flow into plasma from absorptive enterocytes, from macrophages that recycle the iron of senescent erythrocytes, and from hepatocytes that store iron, thereby lowering plasma iron concentrations. Malfunctions of the hepcidin-ferroportin axis contribute to the pathogenesis of different anemias. Deficient production of hepcidin causes systemic iron overload in iron-loading anemias such as beta-thalassemia; whereas hepcidin excess contributes to the development of anemia in inflammatory disorders and chronic kidney disease, and may cause erythropoietin resistance. The diagnosis of different forms of anemia will be facilitated by improved hepcidin assays, and the treatment will be enhanced by the development of hepcidin agonists and antagonists.
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spelling doaj-art-8732bec3e8c04daaa22ab2ccb76596852025-02-03T01:00:34ZengWileyAdvances in Hematology1687-91041687-91122010-01-01201010.1155/2010/750643750643Targeting the Hepcidin-Ferroportin Axis in the Diagnosis and Treatment of AnemiasElizabeta Nemeth0David Geffen School of Medicine at UCLA, CHS 37-131, 10833 LeConte Avenue, Los Angeles, CA 90095-1690, USAThe hepatic peptide hormone hepcidin regulates dietary iron absorption, plasma iron concentrations, and tissue iron distribution. Hepcidin acts by causing the degradation of its receptor, the cellular iron exporter ferroportin. The loss of ferroportin decreases iron flow into plasma from absorptive enterocytes, from macrophages that recycle the iron of senescent erythrocytes, and from hepatocytes that store iron, thereby lowering plasma iron concentrations. Malfunctions of the hepcidin-ferroportin axis contribute to the pathogenesis of different anemias. Deficient production of hepcidin causes systemic iron overload in iron-loading anemias such as beta-thalassemia; whereas hepcidin excess contributes to the development of anemia in inflammatory disorders and chronic kidney disease, and may cause erythropoietin resistance. The diagnosis of different forms of anemia will be facilitated by improved hepcidin assays, and the treatment will be enhanced by the development of hepcidin agonists and antagonists.http://dx.doi.org/10.1155/2010/750643
spellingShingle Elizabeta Nemeth
Targeting the Hepcidin-Ferroportin Axis in the Diagnosis and Treatment of Anemias
Advances in Hematology
title Targeting the Hepcidin-Ferroportin Axis in the Diagnosis and Treatment of Anemias
title_full Targeting the Hepcidin-Ferroportin Axis in the Diagnosis and Treatment of Anemias
title_fullStr Targeting the Hepcidin-Ferroportin Axis in the Diagnosis and Treatment of Anemias
title_full_unstemmed Targeting the Hepcidin-Ferroportin Axis in the Diagnosis and Treatment of Anemias
title_short Targeting the Hepcidin-Ferroportin Axis in the Diagnosis and Treatment of Anemias
title_sort targeting the hepcidin ferroportin axis in the diagnosis and treatment of anemias
url http://dx.doi.org/10.1155/2010/750643
work_keys_str_mv AT elizabetanemeth targetingthehepcidinferroportinaxisinthediagnosisandtreatmentofanemias