The liver-derived peptide hepcidin is the master regulator of systemic iron homeostasis in mammals. Expression depends on multiple signals: extracellular and intracellular iron, inflammation, and erythropoiesis. Bone morphogenetic protein 6 (BMP6) is a key regulator of hepcidin in response to excess iron, via the SMAD pathway, modulated by hemojuvelin, acting as BMP co-receptor. Targeted disruption of the mouse Bmp6 gene was shown to result in a severe iron overload phenotype similar to that of mice deficient for Hamp, which encodes hepcidin, and for Hfe2, which encodes hemojuvelin.

The liver-derived peptide hepcidin is the master regulator of systemic iron homeostasis in mammals. Expression depends on multiple signals: extracellular and intracellular iron, inflammation, and erythropoiesis. Bone morphogenetic protein 6 (BMP6) is a key regulator of hepcidin in response to excess iron, via the SMAD pathway, modulated by hemojuvelin, acting as BMP co-receptor. Targeted disruption of the mouse Bmp6 gene was shown to result in a severe iron overload phenotype similar to that of mice deficient for Hamp, which encodes hepcidin, and for Hfe2, which encodes hemojuvelin.

The liver-derived peptide hepcidin is the master regulator of systemic iron homeostasis in mammals. Expression depends on multiple signals: extracellular and intracellular iron, inflammation, and erythropoiesis. Bone morphogenetic protein 6 (BMP6) is a key regulator of hepcidin in response to excess iron, via the SMAD pathway, modulated by hemojuvelin, acting as BMP co-receptor. Targeted disruption of the mouse Bmp6 gene was shown to result in a severe iron overload phenotype similar to that of mice deficient for Hamp, which encodes hepcidin, and for Hfe2, which encodes hemojuvelin.