Hepcidin and iron metabolism: from laboratory to clinical implications

Abstract

Hepcidin is a liver-synthesized hormone that inhibits the cellular efflux of iron by binding to ferroportin and its subsequent degradation. The main role of hepcidin is regulation of ferroportin expression and cell membrane function. Recent studies implicate hepcidin in a variety of iron disorders in addition to its primary role in the regulation of systemic iron homeostasis. Hepcidin excess has a key pathologic role in anemia of inflammation, chronic kidney disease, and iron-refractory iron deficiency anemia, while hepcidin deficiency is responsible for most cases of familial hemochromatosis and iron-loading anemia. The most important advances on the role of hepcidin in normal and abnormal iron metabolism and the main clinical and diagnostic implications are summarized in this review.