Quantitatively reduced erythropoiesis, limiting iron consumption, increases transferrin saturation and stimulates hepcidin transcription. Expanded erythropoiesis, as after hemorrhage or erythropoietin treatment, blocks hepcidin through an acute reduction of transferrin saturation and the release of the erythroblast hormone and hepcidin inhibitor erythroferrone.
Low hepcidin levels favor bone marrow iron supply for hemoglobin synthesis and red blood cells production. High hepcidin levels block intestinal iron absorption and macrophage iron recycling, causing iron restricted erythropoiesis and anemia.
Hepcidin, the master regulator of systemic iron homeostasis, tightly influences erythrocyte production.
0 kommentar(er)
