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Exploring the role of hepcidin, an antimicrobial and iron regulatory peptide, in increased iron absorption in β-thalassemia

  • Laura Breda
  • , Sara Gardenghi
  • , Ella Guy
  • , Eliezer A. Rachmilewitz
  • , Orly Weizer-Stern
  • , Konstantin Adamsky
  • , Ninette Amariglio
  • , Gideon Rechavi
  • , Patricia J. Giardina
  • , Robert W. Grady
  • , Stefano Rivella
  • Cornell University
  • Edith Wolfson Medical Center Israel
  • Tel Aviv University

Research output: Contribution to journalArticlepeer-review

18 Scopus citations

Abstract

To develop new treatments for β-thalassemia, it is essential to identify the genes involved in the relevant pathophysiological processes. Iron metabolism in thalassemia mice being investigated, focusing on the expression of a gene called hepcidin (Hamp), which is expressed in the liver and whose product (Hamp) is secreted into the bloodstream. In mice, iron overload leads to overespression of Hamp, while Hamp-knockout mice suffer from hemochromatosis. The aim of this study is to investigate Hamp in the mouse model of β-thalassemia and to address the potential gene transfer of Hamp to prevent abnormal iron absorption.

Original languageEnglish
Pages (from-to)417-422
Number of pages6
JournalAnnals of the New York Academy of Sciences
Volume1054
DOIs
StatePublished - 2005
Externally publishedYes

Funding

FundersFunder number
National Institute of Diabetes and Digestive and Kidney DiseasesK01DK063992

    Keywords

    • Gene expression
    • Hamp
    • Iron overload
    • Lentivirus
    • β-thalassemia

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