Multiple relevant targets; primarily Divalent metal-ion transporter 1, Ferroportin 1, Duodenal cytochrome b, Hepcidin, Hypoxia-inducible factor 2α (DMT1, FPN1, DCYTB, HIF-2α)

Intestinal mucosal iron absorption is the process by which dietary iron is selectively taken up by the duodenal villus enterocytes. The predominant pathway for nonheme iron involves reduction of ferric (Fe^3+) to ferrous (Fe^2+) iron (primarily via duodenal cytochrome b), transport across the apical membrane by divalent metal-ion transporter 1 (DMT1), and export from enterocytes into circulation by ferroportin 1. Iron homeostasis is regulated at both systemic (mainly by hepcidin, produced in the liver) and local (mucosal) levels, with cellular mechanisms modulated by hypoxia via hypoxia-inducible factor 2α (HIF-2α). Dysregulation of this process leads to iron deficiency or overload and is implicated in several diseases including anemia, hemochromatosis, and cancers.

Other names

DMT1 (Divalent metal-ion transporter 1; SLC11A2)FPN1 (Ferroportin 1)DCYTB (Duodenal cytochrome b; CYBRD1)HepcidinHIF-2α (EPAS1)

Blockade or enhancement of DMT1-mediated iron uptake; Regulation of ferroportin export (hepcidin binding causes ferroportin degradation); Modulation of hepcidin levels (influences intestinal iron absorption); Stabilization of HIF-2α to increase transcription of iron absorption machinery