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Systemic iron transport and storage proteins comprise a coordinated group of molecules essential for maintaining iron homeostasis in the human body [1, 5]. This system includes transport proteins like transferrin, which shuttles iron through the plasma, and storage proteins like ferritin, which sequesters iron in a non-toxic form within cells [1, 8, 11]. The flux of iron is primarily controlled by the hepcidin-ferroportin axis, where the hormone hepcidin regulates the iron exporter ferroportin to manage iron absorption and recycling [2, 3, 10]. Dysregulation of these proteins is central to various disorders, including hereditary hemochromatosis, characterized by iron overload, and anemia of chronic disease, where iron is sequestered away from erythropoiesis [3, 7, 17]. Pharmacological interventions target these proteins through iron chelation, hepcidin modulation, or direct inhibition of transporters to treat conditions ranging from iron-loading anemias to chronic inflammatory states [2, 9, 12]. These proteins also play roles in cancer progression and neurodegenerative diseases, where iron-mediated oxidative stress contributes to cellular damage [12, 14, 17].
Iron chelation, hepcidin mimetic, hepcidin antagonism, ferroportin inhibition, and iron supplementation.
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