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Pharmaceuticals 2018, 11(4), 127;

Hepcidin Therapeutics

Lady Davis Institute for Medical Research, Jewish General Hospital, Department of Medicine, McGill University, Montreal, QC H3T 1E2, Canada
Author to whom correspondence should be addressed.
Received: 3 November 2018 / Revised: 15 November 2018 / Accepted: 19 November 2018 / Published: 21 November 2018
(This article belongs to the Special Issue Iron as Therapeutic Targets in Human Diseases)
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Hepcidin is a key hormonal regulator of systemic iron homeostasis and its expression is induced by iron or inflammatory stimuli. Genetic defects in iron signaling to hepcidin lead to “hepcidinopathies” ranging from hereditary hemochromatosis to iron-refractory iron deficiency anemia, which are disorders caused by hepcidin deficiency or excess, respectively. Moreover, dysregulation of hepcidin is a pathogenic cofactor in iron-loading anemias with ineffective erythropoiesis and in anemia of inflammation. Experiments with preclinical animal models provided evidence that restoration of appropriate hepcidin levels can be used for the treatment of these conditions. This fueled the rapidly growing field of hepcidin therapeutics. Several hepcidin agonists and antagonists, as well as inducers and inhibitors of hepcidin expression have been identified to date. Some of them were further developed and are currently being evaluated in clinical trials. This review summarizes the state of the art. View Full-Text
Keywords: iron metabolism; hepcidin; ferroportin; hemochromatosis; anemia iron metabolism; hepcidin; ferroportin; hemochromatosis; anemia

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Katsarou, A.; Pantopoulos, K. Hepcidin Therapeutics. Pharmaceuticals 2018, 11, 127.

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