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Systemic iron metabolism encompasses the tightly regulated processes of iron absorption from the diet, transport in the blood (primarily by transferrin), cellular uptake of iron (via transferrin receptor 1 and 2, DMT1, ZIP14), intracellular storage (mainly in ferritin), recycling by macrophages, and regulation by key hormones such as hepcidin[1][3][4][6][7]. Excess or deficiency of iron, and dysregulation of the hepcidin-ferroportin axis, underlie a wide variety of diseases including anemia, hemochromatosis, and conditions affected by oxidative stress. Many individual molecules within these pathways (such as hepcidin, ferroportin, transferrin, and transferrin receptor) are direct therapeutic targets, but the pathway as a whole is a functional concept rather than a druggable entity[1][2][3][4][6][7].\n\nSummary:\n"Systemic Iron Metabolism Pathways" is a physiological concept that collectively refers to many interacting molecules and processes; it is not a single molecular target, and thus cannot be used as one for structured drug-target mapping. Individual components of this pathway (e.g., hepcidin, ferroportin, transferrin receptor 1) are considered therapeutic targets[1][2][3][4][6][7].
Modulation of iron absorption (e.g. via DMT1 inhibition). Inhibition or activation of iron export (e.g. via ferroportin targeting). Hepcidin pathway modulation. Chelation/removal of excess iron.
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