Figure 3
Hypoxia-induced modifications of iron homeostasis. Erythropoietin (EPO) activation is the first event occurring after acute hypoxia exposure, inducing erythropoietic expansion, which requires more iron for red blood cell hemoglobinization. Hepcidin down-regulation is central for this function: it begins within 16 to 40 hours and peaks within a few days of exposure, and thereafter persists for a long time. Iron and erythroid signals cooperate in hepcidin suppression, increasing intestinal iron absorption and cellular iron release. Iron mobilization from stores occurs early, possibly involving a hypoxia-mediated event. Erythroid signal probably requires soluble mediators from bone marrow to the liver. Transferrin saturation (TS) decreased only in the phase of expansion of the erythropoietic mass contributing to hepcidin suppression.

Hypoxia-induced modifications of iron homeostasis. Erythropoietin (EPO) activation is the first event occurring after acute hypoxia exposure, inducing erythropoietic expansion, which requires more iron for red blood cell hemoglobinization. Hepcidin down-regulation is central for this function: it begins within 16 to 40 hours and peaks within a few days of exposure, and thereafter persists for a long time. Iron and erythroid signals cooperate in hepcidin suppression, increasing intestinal iron absorption and cellular iron release. Iron mobilization from stores occurs early, possibly involving a hypoxia-mediated event. Erythroid signal probably requires soluble mediators from bone marrow to the liver. Transferrin saturation (TS) decreased only in the phase of expansion of the erythropoietic mass contributing to hepcidin suppression.

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