( We all know that iron deficiencies are ...)Putting an old drug to a new use

We all know that iron deficiencies are dangerous, but also too much iron is bad for our health. Our body stores excess iron in various tissues, where it can lead to organ failure and even death if not treated before irreversible damage has occurred. Researchers from the Innsbruck Medical University, the University of Heidelberg, Germany, and the European Molecular Biology Laboratory (EMBL) now made a surprising discovery that may lead to new therapeutic approaches to treating such disorders. In this week's online issue of the journal Nature Medicine they report that a compound that was frequently used to treat high blood pressure can reverse iron overload in mouse models and has the potential to treat similar conditions in humans.

Our body needs most of its iron to make red blood cells. A lack of the metal can lead to dangerous anemias, but also too much iron can be detrimental as iron promotes the formation of toxic radicals leading to tissue damage. Iron overload is the consequence of one of the most common genetic disorders in Europe, hereditary hemochromatosis, which affects about one in 300 Europeans. Excess iron also accumulates after repeated blood transfusions and can cause organ failure over time. Günter Weiss, a clinician from the Innsbruck Medical University, and his collaborators from the University of Heidelberg and EMBL now found out that nifedipine, a substance commonly used to control blood pressure, helps the body deal with too much iron.

"We observed in mice with iron overload that nifedipine helps mobilise iron from stores in the liver and enhances its excretion into the urine," says Weiss, an EMBL alumnus who now heads a lab at the Department for General Internal Medicine at the University of Innsbruck. "These effects make nifedipine a promising candidate for a new drug to treat hereditary hemochromatosis and other iron overload disorders."

Combining electrophysiology, cell biology and molecular investigations, Weiss an
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Source:European Molecular Biology Laboratory

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