• Susana Conde Diez, Ricardo de Las Cuevas Allende, and Eulogio Conde García.
• Medicina de Familia, Servicio Cántabro de Salud, Santander (Cantabria), España.
• Med Clin (Barc). 2017 Mar 3; 148 (5): 218224218-224.

AbstractHepcidin 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 synthesised 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.Copyright © 2016 Elsevier España, S.L.U. All rights reserved.

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