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The iron transport pathway is a critical physiological system that regulates the acquisition, distribution, and storage of iron, an essential element for oxygen transport and DNA synthesis (NIH, 2013). Key components include transferrin, which transports iron in the blood, and transferrin receptor 1 (TfR1), which facilitates cellular uptake via endocytosis (NIH, 2013). Ferroportin serves as the sole known cellular iron exporter, and its activity is tightly regulated by the hormone hepcidin, which induces its degradation to lower plasma iron levels (ResearchGate, 2013). Dysregulation of this pathway is central to various diseases, including iron deficiency anemia and iron overload disorders like hereditary hemochromatosis (NIH, 2019). Therapeutic strategies targeting this pathway range from iron supplementation and chelation therapy to novel hepcidin mimetics and ferroportin inhibitors designed to restore iron homeostasis (NIH, 2019). Additionally, the pathway is increasingly recognized as a target in cancer and neurodegenerative diseases, where iron-mediated oxidative stress and ferroptosis play significant roles (NIH, 2019; MDPI, 2023).
The iron transport pathway is modulated through various mechanisms: iron supplementation increases available iron; chelation therapy removes excess iron; hepcidin mimetics or ferroportin inhibitors restrict iron export into the plasma; and erythropoiesis-stimulating agents increase iron utilization (NIH, 2013; NIH, 2019).
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