Iron-Overload–Related Disease in HFE Hereditary Hemochromatosis

نویسندگان

  • Katrina J. Allen
  • Dorota M. Gertig
چکیده

Katrina J. Allen, M.D., Ph.D., Lyle C. Gurrin, Ph.D., Clare C. Constantine, Ph.D., Nicholas J. Osborne, Ph.D., Martin B. Delatycki, M.D., Ph.D., Amanda J. Nicoll, M.D., Ph.D., Christine E. McLaren, Ph.D., Melanie Bahlo, Ph.D., Amy E. Nisselle, B.Sc., Chris D. Vulpe, M.D., Ph.D., Gregory J. Anderson, Ph.D., Melissa C. Southey, Ph.D., Graham G. Giles, Ph.D., Dallas R. English, Ph.D., John L. Hopper, Ph.D., John K. Olynyk, M.D., Lawrie W. Powell, M.D., Ph.D., and Dorota M. Gertig, M.D., D.Sc.

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Molecular basis of HFE-hemochromatosis

Iron-overload disorders owing to genetic misregulation of iron acquisition are referred to as hereditary hemochromatosis (HH). The most prevalent genetic iron overload disorder in Caucasians is caused by mutations in the HFE gene, an atypical MHC class I molecule. Recent studies classified HFE/Hfe-HH as a liver disease with the primarily failure in the production of the liver iron hormone hepci...

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OBJECTIVE Excess tissue iron levels are a risk factor for diabetes, but the mechanisms underlying the association are incompletely understood. We previously published that mice and humans with a form of hereditary iron overload, hemochromatosis, exhibit loss of β-cell mass. This effect by itself is not sufficient, however, to fully explain the diabetes risk phenotype associated with all forms o...

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تاریخ انتشار 2008