Figure 1.

Iron metabolism. (A) Iron absorption. DCYTB mediates the conversion of dietary non-heme iron (Fe³⁺) to ferrous ion (Fe²⁺), which is then absorbed by DMT1 in the membrane of intestinal epithelial cells. Following this intake, iron is either retained in ferritin or transferred to the basement membrane by the iron-chaperone PCBP2, where it is subsequently converted to Fe³⁺ by hephaestin. Finally, iron is discharged to the portal circulation through FPN. Tf attaches to the exported iron, which is then transported to numerous peripheral tissues. HRG-1 may uptake heme through endocytosis. Heme is degraded by heme oxygenase once it has been absorbed. Similar to the transport of non-heme iron, iron liberated from heme is transferred to portal vein blood through FPN. (B) Iron distribution. Hepcidin regulates the production of FPN by directly binding to FPN and promoting its breakdown, thus facilitating the transport of iron to the portal vein. Iron is mainly distributed in red blood cells, which transport oxygen in the blood, and tissues, such as muscle, liver and bone marrow. DCYTB, duodenal cytochrome b; DMT1, divalent metal transporter 1; PCBP2, poly(C)-binding protein 2; FPN, ferroportin; HRG-1, heme responsive gene-1; Tf, transferrin.