

Beta-thalassemia is an inherited blood disorder that results in chronic anaemia. 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 anaemia. They therefore suggest that therapeutic approaches that increase hepcidin levels in patients with beta-thalassemia could be therapeutic, limiting iron overload and mitigating anaemia.
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.
Site for alcohol's action in the brain discovered
The battle for CRTC2: How obesity increases the risk for diabetes
Cancer: The cost of being smarter than chimps?
Study gives clues to how adrenal cancer forms