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*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

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

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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