Iron transport and storage system (Endogenous)

The endogenous iron transport and storage system refers to the coordinated network of proteins responsible for the absorption, transport, cellular uptake, storage, and recycling of iron. Dietary iron is absorbed by enterocytes in the small intestine via divalent metal transporter 1 (DMT1). Export into blood is mediated by ferroportin and iron is oxidized and bound to transferrin for transport[1][2][5]. Cells take up transferrin-bound iron via the transferrin receptor which delivers iron via endocytosis, after which it is released into the cytoplasm by DMT1[2][5]. Excess iron is stored in ferritin or hemosiderin; recycling takes place via macrophages. Regulation is exquisitely controlled by hepcidin, which inhibits ferroportin-mediated iron export, and by cellular proteins such as IRP1/2 and iron-responsive elements to modulate translation of related transporters and storage proteins[1][4][5]. Dysfunction of these processes underlies iron deficiency anemia, hereditary hemochromatosis, and contributes to cancer, infection risk, and neurodegeneration. Key molecular components: - Transferrin (iron transporter in plasma)[2][5] - Transferrin receptor (TfR1) (cellular iron import, receptor)[2][5] - Divalent metal transporter 1 (DMT1) (intestinal/cellular iron import)[5] - Ferroportin (iron export)[1][5] - Ferritin (iron storage)[2][5] - Hepcidin (systemic regulatory hormone)[1][5] - Ferrireductases and ferroxidases (oxidation/reduction during transport)[1][7] Because this query refers to a whole system and not a specific molecule/receptor, the response is flagged "is_incorrect: true" and "is_target: false": drug therapy is directed to components or their pathways, not the collective system itself. For structured data, focus on specific proteins such as “Transferrin receptor 1” or “Ferroportin” when targeting iron metabolism therapeutically.

Other names

Iron homeostasis systemIron metabolism pathwayIron transport and storage pathway

Chelation of systemic or intracellular iron to reduce toxicity (chelator drugs) - Delivery of iron for uptake during deficiency (iron supplementation) - Modulation of protein function to restore iron transport/export (e.g. hinokitiol bypassing defective endogenous transporters)