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Acta bioquímica clínica latinoamericana

versão impressa ISSN 0325-2957versão On-line ISSN 1851-6114

Resumo

NUCIFORA, Elsa Mercedes. Hepcidin: the key of iron metabolism. Acta bioquím. clín. latinoam. [online]. 2017, vol.51, n.3, pp.375-378. ISSN 0325-2957.

In the last decades, a lot of progress has been made on the knowledge of iron (Fe) metabolism regulation. Hepcidin (Hp) is produced by hepatocytes and it regulates the iron absorption from the duodenum and the liberation from macrophages and from the liver. When there is iron deficiency, Hp, which delivers iron to transferrin (Tf), is low. Iron overload and inflammation cytokines stimulate Hp production. The Hp natural executor is Ferroportin (FP), which is the only iron exporter from the cells. One of the natural regulators of Hp is Matriptasa 2, which down regulates Hp. Mutations that limit their expression induce iron overload and anemia (IRIDA). In the last few years, Erythroferrone (ERFE) was discovered. ERFE is produced by active erythroblasts: it inhibits Hp synthesis, allowing the iron liberation from deposits and its duodenal absorption, and also the iron release from macrophages facilitating the erythroid production. The erythroblastic activity, even ineffective, acts as a stimulus of ERFE synthesis. Until now, it has not been defined yethow these different variables could be used for diagnosis, its standardization, or for therapeutic applications, but it is highly probable that they will improve our knowledge and managements kills in this field.

Palavras-chave : Hepcidin; Iron; Ferroportin; Matriptasa ii; Erythropoyetin; Erythroferrone.

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