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Hepcidin and Hfe in iron overload in beta-thalassemia.

Abstract
Hepcidin (HAMP) negatively regulates iron absorption, degrading the iron exporter ferroportin at the level of enterocytes and macrophages. We showed that mice with beta-thalassemia intermedia (th3/+) have increased anemia and iron overload. However, their hepcidin expression is relatively low compared to their iron burden. We also showed that the iron metabolism gene Hfe is down-regulated in concert with hepcidin in th3/+ mice. These observations suggest that low hepcidin levels are responsible for abnormal iron absorption in thalassemic mice and that down-regulation of Hfe might be involved in the pathway that controls hepcidin synthesis in beta-thalassemia. Therefore, these studies suggest that increasing hepcidin and/or Hfe expression could be a strategy to reduces iron overload in these animals. The goal of this paper is to review recent findings that correlate hepcidin, Hfe, and iron metabolism in beta-thalassemia and to discuss potential novel therapeutic approaches based on these recent discoveries.
AuthorsSara Gardenghi, Pedro Ramos, Antonia Follenzi, Niva Rao, Eliezer A Rachmilewitz, Patricia J Giardina, Robert W Grady, Stefano Rivella
JournalAnnals of the New York Academy of Sciences (Ann N Y Acad Sci) Vol. 1202 Pg. 221-5 (Aug 2010) ISSN: 1749-6632 [Electronic] United States
PMID20712796 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't, Review)
Chemical References
  • Anti-Bacterial Agents
  • Antimicrobial Cationic Peptides
  • HAMP protein, human
  • HFE protein, human
  • Hamp protein, mouse
  • Hemochromatosis Protein
  • Hepcidins
  • Histocompatibility Antigens Class I
  • Membrane Proteins
Topics
  • Anemia (etiology, metabolism)
  • Animals
  • Anti-Bacterial Agents (metabolism, therapeutic use)
  • Antimicrobial Cationic Peptides (genetics, metabolism, therapeutic use)
  • Genetic Therapy
  • Genetic Vectors (genetics)
  • Hemochromatosis Protein
  • Hepcidins
  • Histocompatibility Antigens Class I (genetics, metabolism, therapeutic use)
  • Humans
  • Iron Overload (etiology, metabolism, therapy)
  • Membrane Proteins (genetics, metabolism, therapeutic use)
  • beta-Thalassemia (complications, genetics, metabolism, therapy)

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