Beta-thalassemia is an inherited blood disorder that results in chronic anemia. A major complication of the condition is iron overload, which damages organs such as the liver and heart. The iron overload has been linked to low levels of the protein hepcidin, a negative regulator of intestinal iron absorption and iron recycling. A team of researchers, led by Stefano Rivella, at Weill Cornell Medical College, New York, has now shown that increasing the concentration of hepcidin in beta-thalassemic mice limits iron overload and markedly reduces their anemia. They therefore suggest that therapeutic approaches that increase hepcidin levels in patients with beta-thalassemia could be therapeutic, limiting iron overload and mitigating anemia.
In an accompanying commentary, Mark Fleming and Thomas Bartnikas, at Children's Hospital Boston, discuss these data and suggest that modulating hepcidin levels could be a new approach to treating a multitude of diseases associated with iron overload or deficiency.
TITLE: Hepcidin as a therapeutic tool to limit iron overload and improve anemia in beta-thalassemic mice
Weill Cornell Medical College, New York, New York, USA.
Phone: 212.746.4941; Fax: 212.746.8423; E-mail: email@example.com.
View this article at: http://www.jci.org/articles/view/41717?key=c4981adf3d5ea08a7e57
TITLE: A tincture of hepcidin cures all: the potential for hepcidin therapeutics
Mark D. Fleming
Children's Hospital Boston, Boston, Massachusetts, USA.
Phone: 617.919.2664; Fax: 617.730.0168; E-mail: firstname.lastname@example.org.
View this article at: http://www.jci.org/articles/view/45043?key=a84ffb2845dc5e10e863
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