Exploring the Role of Hepcidin, an Antimicrobial and Iron Regulatory Peptide, in Increased Iron Absorption in ?-Thalassemia
Abstract: To develop new treatments for ?-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 overexpression of Hamp, while Hamp-knockout mice suffer from hemochromatosis. The aim of this study is to investigate Hamp in the mouse model of ?-thalassemia and to address the potential gene transfer of Hamp to prevent abnormal iron absorption.
?-thalassemia hamp iron overload gene expression lentivirus