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Iron is a chemical element (symbol Fe) essential for life, required as a cofactor in proteins involved in oxygen transport, mitochondrial electron transfer, DNA synthesis, and cell cycle regulation. Iron is not a molecular "receptor" or "target" but is implicated as a central component or cofactor in numerous proteins that serve as therapeutic targets, such as those regulating iron homeostasis, redox balance, and ferroptosis. Iron dysregulation is involved in many diseases, and both iron chelators and iron supplements are clinically used drugs for managing iron overload and deficiency, respectively. Iron modulation (e.g., through ferroptosis) is being explored as a therapeutic approach in cancer and neurodegenerative disease[3][4][5][6][7]. Additional context: - Ferroptosis is an iron-dependent form of regulated cell death characterized by lipid peroxidation, and therapeutic efforts seek to either induce (as in cancer) or inhibit (as in neurodegeneration) ferroptosis by targeting iron metabolism[4][5][6][7]. - Although many drugs interact with iron, in most cases they do so by chelating or supplementing iron, rather than specifically binding to a single iron target protein or receptor[3][5][6].
Chelation of iron to reduce its bioavailability and prevent toxic overload[3][5][6] Supplementation to correct deficiency (iron salts, intravenous iron)[3][5] Modulation of ferroptosis sensitivity or resistance[4][5][7]
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