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Prepublished online as a Blood First Edition Paper on March 27, 2003; DOI 10.1182/blood-2003-03-0672. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-03-0672v1 102/3/783    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Ganz, T. Search for Related Content PubMed PubMed Citation Articles by Ganz, T. Related Collections Red Cells Review Articles Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 August 2003, Vol. 102, No. 3, pp. 783-788 REVIEW ARTICLES Hepcidin, a key regulator of iron metabolism and mediator of anemia of inflammation Tomas Ganz From the Departments of Medicine and Pathology, David Geffen School of Medicine, University of California, Los Angeles, CA Human hepcidin, a 25–amino acid peptide made by hepatocytes, may be a new mediator of innate immunity and the long-sought iron-regulatory hormone. The synthesis of hepcidin is greatly stimulated by inflammation or by iron overload. Evidence from transgenic mouse models indicates that hepcidin is the predominant negative regulator of iron absorption in the small intestine, iron transport across the placenta, and iron release from macrophages. The key role of hepcidin is confirmed by the presence of nonsense mutations in the hepcidin gene, homozygous in the affected members, in 2 families with severe juvenile hemochromatosis. Recent evidence shows that deficient hepcidin response to iron loading may contribute to iron overload even in the much milder common form of hemochromatosis, from mutations in the HFE gene. In anemia of inflammation, hepcidin production is increased up to 100-fold and this may account for the defining feature of this condition, sequestration of iron in macrophages. The discovery of hepcidin and its role in iron metabolism could lead to new therapies for hemochromatosis and anemia of inflammation. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Unlocking the mysteries of iron homeostasis and of the anemia of chronic disease: is hepcidin the key? Ernest Beutler Blood 2003 102: 775. 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