Journal
HAEMATOLOGICA
Volume 98, Issue 11, Pages 1667-1676Publisher
FERRATA STORTI FOUNDATION
DOI: 10.3324/haematol.2013.084624
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Funding
- NIDDK NIH HHS [R01 DK090554] Funding Source: Medline
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Hepcidin, the liver-produced peptide hormone, is a principal regulator of iron homeostasis. Abnormal hepcidin production has emerged as a causative factor in several common iron disorders. Hepcidin insufficiency results in iron overload in hereditary hemochromatosis and iron-loading anemias, whereas hepcidin excess causes or contributes to the development of iron-restricted anemias in inflammatory diseases, infections, some cancers and chronic kidney disease. Not surprisingly, hepcidin and related pathways have become the target for the development of novel therapeutics for iron disorders. In this review, we will summarize the strategies and development programs that have been devised for agonizing or antagonizing hepcidin and its receptor ferroportin.
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