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Systemic iron-utilisation pathways encompass the coordinated physiological processes that regulate the absorption, transport, storage, and recycling of iron to maintain homeostasis. The master regulator of these pathways is hepcidin, a peptide hormone that controls the systemic flux of iron by modulating the levels of ferroportin, the only known cellular iron exporter. These pathways are essential for vital functions such as erythropoiesis, where iron is incorporated into hemoglobin, and cellular respiration. Dysregulation of iron utilization is central to the pathogenesis of various disorders, including iron deficiency anemia, anemia of chronic disease, and hereditary hemochromatosis. Therapeutic interventions targeting these pathways include iron chelators to remove excess iron, hepcidin mimetics to treat iron overload or polycythemia, and HIF-prolyl hydroxylase inhibitors to enhance iron mobilization for red blood cell production. Monitoring of these pathways is clinically achieved through biomarkers such as serum ferritin, transferrin saturation, and hepcidin levels.
Modulation of systemic iron levels through the regulation of iron absorption in the gut, recycling by macrophages, and storage in the liver, primarily via the hepcidin-ferroportin axis or direct iron chelation.
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