Hepcidin plays a central role in the regulation of iron homeostasis. It is produced in the liver, processed, and secreted as hepcidin-25. More recent studies have also suggested that hepcidin (PLP-4392-s) can be produced by macrophages, fat cells, cardiomyocytes, and pancreatic beta cells. Hepcidin regulates iron by binding to the iron exporter ferroportin, leading to its internalization and degradation. In turn, release of iron by macrophages is inhibited and iron uptake is decreased in the gut. Events such as inflammation and high concentrations of stored iron can trigger increase in hepcidin production while events such as iron deficiency, anemia, hypoxia, and erythropoiesis can trigger a decrease in production.
Recent studies collectively suggest hepcidin may become an important part of diagnosis, monitoring, and treatment of diseases. Chronic kidney disease (CKD) can result in inflammation, erythropoiesis, lower iron levels, anemia and hypoxia, which in turn can influence hepcidin levels in patients. The influence of hepcidin levels in patients with iron deficiency anemia and anemia of chronic disease indicates the peptide may be a possible marker for detection of disease. In anemia and hypoxia, erythropoietin (EPO) or iron can be used for treatment, which in turn can influence hepcidin levels in plasma. As a result, monitoring of hepcidin levels can be used to help determine the effectiveness of these treatment strategies. Hemochromatosis is an iron overload disease where hepcidin may also be important for screening and monitoring of disease. necessary to fully determine the usefulness of hepcidin as a tool for screening, diagnosis, and treatment of disease.