This project is funded by the Croatian Science Foundation.
Development of novel antibodies (biologics) that will selectively inhibit hepcidin expression in the liver for the Treatment of Anemia of Chronic Disease
(BMP6Fe3)
Research Project
In this project, we will focus on understanding specified features of BMP6 biology on regulation of serum iron to develop a novel therapy for anemia of chronic disease (ACD), an unmet medical need.
Figure 1. Schematic representation of hepcidin expression in hepatocytes in response to iron levels. Hepcidin expression in hepatocytes is controlled by BMP6 signaling cascade, HJV, neogenin, TfR2 and HFE. Low iron conditions (a) promote MT2 induced cleavage of HJV, destabilize TfR2/HFE interaction and reduce BMP6 secretion from the non-parenchymal cells thus reducing BMP signaling and lowering hepcidin expression. High iron conditions (b) increase loading of Tf with iron, stabilize TfR2/HFE interaction and induce BMP6 secretion from non-parenchymal cells. This in turn leads to the formation of BMP6/BMPR/HJV/neogenin/TfR2 /HFE complex which enhances hepcidin expression in hepatocytes. Prepared by M. Matijasic for this project.
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