Hepcidin regulation: ironing out the details

Department of Pathology, University of Utah School of Medicine, Salt Lake City, Utah, USA.

Address correspondence to: Jerry Kaplan, Department of Pathology, University of Utah School of Medicine, 50 North Medical Drive, Salt Lake City, Utah 84106, USA. Phone: (801) 581-7427; Fax: (801) 581-4517; E-mail: ude.hatu.htap@nalpak.yrrej.

Department of Pathology, University of Utah School of Medicine, Salt Lake City, Utah, USA.

Abstract

Hepcidin is a peptide hormone secreted by the liver that plays a central role in the regulation of iron homeostasis. Increased hepcidin levels result in anemia while decreased expression is the causative feature in most primary iron overload diseases. Mutations in hemochromatosis type 2 (HFE2), which encodes the protein hemojuvelin (HJV), result in the absence of hepcidin and an early-onset form of iron overload disease. HJV is a bone morphogenetic protein (BMP) coreceptor and HJV mutants have impaired BMP signaling. In this issue of the JCI, Babitt and colleagues show that BMPs are autocrine hormones that induce hepcidin expression (see the related article beginning on page 1933). Administration of a recombinant, soluble form of HJV decreased hepcidin expression and increased serum iron levels by mobilizing iron from splenic stores. These results demonstrate that recombinant HJV may be a useful therapeutic agent for treatment of the anemia of chronic disease, a disorder resulting from high levels of hepcidin expression.

Abstract

Acknowledgments

The research work in the laboratory of J. Kaplan is supported by NIH grants DK070947 and DK30534. The authors express their appreciation to Richard Ajioka for assistance with Figure Figure2. 2.

Acknowledgments

Footnotes

Nonstandard abbreviations used: BMP, bone morphogenetic protein; HJV, hemojuvelin.

Conflict of interest: The authors have declared that no conflict of interest exists.

Citation for this article:J. Clin. Invest.117:1755–1758 (2007). doi:10.1172/JCI32701.

See the related article beginning on page 1933.

Footnotes

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