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Cellular iron homeostasis describes the highly regulated processes controlling iron uptake, storage, utilization, and export within cells, involving key molecules such as transferrin receptor 1, divalent metal transporter 1 (DMT1), ferroportin, ferritin, and regulation by the iron-responsive element/iron regulatory protein (IRE/IRP) system[1][6]. This pathway is central for essential cellular functions (DNA synthesis, mitochondrial respiration, oxygen transport) but must be balanced to prevent iron toxicity through reactive oxygen species generation[7][1]. Dysregulation leads to various diseases and enables cell death via ferroptosis, an iron-dependent, non-apoptotic process characterized by lipid peroxidation and implicated in cancer and neurodegeneration[5]. The pathway is not a single molecular entity but a network of proteins and signals[6][7]. Therapeutic interventions target specific proteins (e.g., hepcidin modulators, iron chelators), not the pathway itself. Hence, "Cellular iron homeostasis / Ferroptosis pathway" is not a canonical drug target but an umbrella term for multiple, more specific molecular targets.
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