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Inicio Medicina Clínica (English Edition) Current status of iron metabolism: Clinical and therapeutic implications
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Vol. 148. Issue 5.
Pages 218-224 (March 2017)
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Vol. 148. Issue 5.
Pages 218-224 (March 2017)
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DOI: 10.1016/j.medcle.2017.03.001
Current status of iron metabolism: Clinical and therapeutic implications
Estado actual del metabolismo del hierro: implicaciones clínicas y terapéuticas
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Susana Conde Dieza, Ricardo de las Cuevas Allendeb, Eulogio Conde Garcíac,
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euconde@humv.es
condee@unican.es

Corresponding author.
a Medicina de Familia, Servicio Cántabro de Salud, Santander (Cantabria), Spain
b Medicina de Familia, Servicio Cántabro de Salud, Centro de Salud Bajo Asón, Ampuero (Cantabria), Spain
c Servicio de Hematología, Hospital Universitario Marqués de Valdecilla, Universidad de Cantabria, Santander (Cantabria), Spain
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Table 1. Hepcidin inhibitors and their corresponding targets.
Abstract

Hepcidin is the main regulator of iron metabolism and a pathogenic factor in iron disorders. Hepcidin deficiency causes iron overload, whereas hepcidin excess causes or contributes to the development of iron-restricted anaemia in chronic inflammatory diseases. We know the mechanisms involved in the synthesis of hepcidin and, under physiological conditions, there is a balance between activating signals and inhibitory signals that regulate its synthesis. The former include those related to plasmatic iron level and also those related to chronic inflammatory diseases. The most important inhibitory signals are related to active erythropoiesis and to matriptase-2. Knowing how hepcidin is synthesized has helped design new pharmacological treatments whose main target is the hepcidin. In the near future, there will be effective treatments aimed at correcting the defect of many of these iron metabolism disorders.

Keywords:
Iron metabolism
Hepcidin
Ferroportin
Hepcidin agonists
Hepcidin antagonists
Resumen

La hepcidina es el principal regulador del metabolismo del hierro y el factor patogénico más importante en sus trastornos. La deficiencia de hepcidina provoca sobrecarga de hierro, mientras que su exceso da lugar o contribuye al desarrollo de anemias por déficit o restricción de hierro en las enfermedades crónicas. Conocemos los mecanismos implicados en la síntesis de hepcidina y, en condiciones fisiológicas, hay un equilibrio entre las señales activadoras e inhibidoras que regulan su síntesis. Las primeras incluyen las relacionadas con la concentración plasmática de hierro y con las enfermedades inflamatorias. Las señales inhibidoras más importantes están relacionadas con la eritropoyesis activa y con la matriptasa-2. Conocer cómo se sintetiza la hepcidina ha servido para diseñar nuevos tratamientos farmacológicos cuya diana principal es la hepcidina. En un futuro próximo, se dispondrá de tratamientos eficaces dirigidos a corregir el defecto de muchos de los trastornos del metabolismo del hierro.

Palabras clave:
Metabolismo del hierro
Hepcidina
Ferroportina
Agonistas de la hepcidina
Antagonistas de la hepcidina

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