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The "physiological iron transport and storage system" is not a single target, but encompasses the integrated network of proteins and regulatory molecules responsible for dietary iron absorption, vascular transport of iron, cellular uptake, storage, release, recycling, and regulation. The main plasma transporter is transferrin, which binds ferric iron and delivers it to cells expressing transferrin receptor 1 (TFR1) through receptor-mediated endocytosis. Iron is reduced and transported into the cytosol by DMT1, stored safely in ferritin or hemosiderin, and exported by ferroportin—the only known iron exporter—whose levels are regulated by the liver-derived hormone hepcidin. Multiple enzymes, transporters, and storage proteins collaborate to maintain iron homeostasis, and dysregulation leads to common human diseases such as anemia and iron overload disorders[1][2][3][5][7].\n\nKey supporting details:\n- Multiple distinct molecules and pathways participate in iron transport/storage, each with its own structure and therapeutic relevance[1][2][3][7].\n- No single protein named "Physiological Iron Transport and Storage System" is recognized in the literature; search for this as a target yields references to the broader process/system, not a molecule.\n- Diagnostic and therapeutic interventions target individual components of this system, not the system itself as a unique entity (e.g., targeting hepcidin, transferrin receptor, DMT1, ferroportin, etc.)[1][2][5].\n- Common biomarkers (e.g., ferritin, transferrin saturation, soluble transferrin receptor) reflect the functioning of this system, not any single molecule[2][3][7].\n\nIf your use case requires a specific protein, transporter, or receptor, please specify (e.g., "Transferrin receptor 1," "Ferroportin," "Ferritin") for structured information on that canonical target.
Chelation of free or stored iron (iron chelators)\nModulation of iron absorption/export (via hepcidin agonists/antagonists)\nSupplementation to correct deficiency (iron salts)
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