Blood Res 2013; 48(1):
Published online March 31, 2013
https://doi.org/10.5045/br.2013.48.1.10
© The Korean Society of Hematology
Ematologia/Coagulazione, Laboratorio di Chimica-Clinica, Ematologia e Microbiologia, Azienda Ospedaliera S.Antonio Abate di Callarate, Varese, Italy.
Correspondence to : Correspondence to Guido D'Angelo, M.D. Laboratorio di Chimica-Clinica, Ematologia e Microbiologia, Azienda Ospedaliera S.Antonio Abate di Callarate, Via Pastori 4, 21013, Gallarate, Varese, Italy. Tel: +39-0331-751-456, Fax: +39-0331-751-124, guido.dangelo@aogalalrate.it
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
This review summarizes the central role of hepcidin in the iron homeostasis mechanism, the molecular mechanism that can alter hepcidin expression, the relationship between hepcidin and erythropoiesis, and the pathogenetic role of hepcidin in different types of anemia. In addition, the usefulness of hepcidin dosage is highlighted, including the problems associated with analytical methods currently used as well as the measures of its molecular isoforms. Considering the central role of hepcidin in iron arrangement, it is reasonable to ponder its therapeutic use mainly in cases of iron overload. Further clinical trials are required before implementation.
Keywords Anemia, Hepcidin, Ferroportin, Hepcidin measurement, Hepcidin agonist therapy
Blood Res 2013; 48(1): 10-15
Published online March 31, 2013 https://doi.org/10.5045/br.2013.48.1.10
Copyright © The Korean Society of Hematology.
Guido D'Angelo*
Ematologia/Coagulazione, Laboratorio di Chimica-Clinica, Ematologia e Microbiologia, Azienda Ospedaliera S.Antonio Abate di Callarate, Varese, Italy.
Correspondence to: Correspondence to Guido D'Angelo, M.D. Laboratorio di Chimica-Clinica, Ematologia e Microbiologia, Azienda Ospedaliera S.Antonio Abate di Callarate, Via Pastori 4, 21013, Gallarate, Varese, Italy. Tel: +39-0331-751-456, Fax: +39-0331-751-124, guido.dangelo@aogalalrate.it
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
This review summarizes the central role of hepcidin in the iron homeostasis mechanism, the molecular mechanism that can alter hepcidin expression, the relationship between hepcidin and erythropoiesis, and the pathogenetic role of hepcidin in different types of anemia. In addition, the usefulness of hepcidin dosage is highlighted, including the problems associated with analytical methods currently used as well as the measures of its molecular isoforms. Considering the central role of hepcidin in iron arrangement, it is reasonable to ponder its therapeutic use mainly in cases of iron overload. Further clinical trials are required before implementation.
Keywords: Anemia, Hepcidin, Ferroportin, Hepcidin measurement, Hepcidin agonist therapy
Inflammation increases interleukin-6 production. The consequent increase in hepcidin blocks macrophage iron release as well as the intestinal absorption of iron, resulting in hypoferremia. Abbreviations: TF, transferrin; Fe, iron; DMT1, divalent metal transporter 1.
Pathophysiology of hemochromatosis and anemia of chronic disease.
Table 1 . Hepcidin levels and other iron-related parameters in various types of anemia..
Jeong Suk Koh and Ik‑Chan Song
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Inflammation increases interleukin-6 production. The consequent increase in hepcidin blocks macrophage iron release as well as the intestinal absorption of iron, resulting in hypoferremia. Abbreviations: TF, transferrin; Fe, iron; DMT1, divalent metal transporter 1.
|@|~(^,^)~|@|Pathophysiology of hemochromatosis and anemia of chronic disease.