A growth factor involved in inducing bone formation has an unsuspected role in iron metabolism, according to two studies published online this week in Nature Genetics.
Genetic hemochromatosis is a disorder caused by mutations in genes that encode the major iron regulatory hormone hepcidin and a cell surface receptor called hemojuvelin. Independent studies carried out by Marie-Paule Roth and by Jodie Babitt now show that in response to sensing iron levels, BMP6, a protein known previously to induce the formation of bone and cartilage, binds the hemojuvelin receptor to stimulate the release of the liver hormone hepcidin in order to prevent iron overload in mice.
The sustained deficiency of hepcidin causes excessive iron absorption from the diet and leads to the deposition of iron in the liver and other tissues, which in turn results in organ damage functional failure. These characteristics were similarly observed in mice with targeted disruption of the Bmp6 gene which resulted in massive iron overload in the liver, heart and pancreas.
It remains to be seen how iron regulates Bmp6 expression, which in turn will augment our understanding of how iron affects hepcidin expression. However, while patients with BMP6 mutations have yet to be described, drugs that act in a similar manner to BMP6 may be a useful alternative treatment strategy for managing iron-overload disorders.
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