Abstract
Hepcidin, a 25 amino acid liver-derived peptide, has been recognized as a regulator of iron homeostasis. Hepcidin levels are negatively correlated with erythropoietic expansion, consistent with erythrocytes representing the major compartment that utilizes iron and hepcidin the major regulator for limiting iron availability (Nemeth, 2008). However, the molecular pathway transmitting the signal from proliferating erythrocytes to the regulation of hepcidin expression in hepatocytes has not been clearly defined.
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