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The iron metabolic pathway constitutes the full network of proteins, enzymes, transporters, and regulatory molecules that together control the uptake, utilization, storage, and systemic distribution of iron in the body. At the systemic level, hepcidin (a liver-derived peptide hormone) serves as the master regulator by modulating absorption of dietary iron via duodenal enterocytes and release from macrophages and hepatocytes through the iron exporter ferroportin. Cellular iron homeostasis is controlled by the post-transcriptional interactions between iron regulatory proteins (IRP1, IRP2) and iron-responsive elements (IREs) in the mRNA of target genes, governing the synthesis of ferritin (storage protein), transferrin receptor (iron importer), and other factors. This regulation allows for balanced iron supply essential for processes such as oxygen transport (hemoglobin), mitochondrial respiration, and DNA synthesis, while protecting tissues from iron-induced oxidative toxicity. Dysregulation of any component in this pathway can contribute to a wide array of human diseases, including anemias, iron overload syndromes like hemochromatosis, neurodegenerative conditions, and altered immune responses
Depends on the component targeted: - Chelators bind free iron, reducing bioavailability and preventing toxicity. - Supplements provide biologically available iron. - Hepcidin modulators alter iron export via ferroportin regulation. - Transferrin receptor antagonists limit iron uptake in specific cells
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