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 language | English |
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Pages (from-to) | 417-422 |
Number of pages | 6 |
Journal | Annals of the New York Academy of Sciences |
Volume | 1054 |
DOIs | |
State | Published - 2005 |
Externally published | Yes |
Keywords
- Gene expression
- Hamp
- Iron overload
- Lentivirus
- β-thalassemia