Hepcidin-ferroportin pathway

The **hepcidin-ferroportin pathway** is a regulatory axis central to the control of systemic iron homeostasis. Hepcidin, a 25-amino acid peptide hormone primarily produced by the liver, regulates iron metabolism by binding to ferroportin, the only known cellular iron exporter located on enterocytes, macrophages, and hepatocytes. On binding, hepcidin induces ferroportin internalization and degradation, thereby blocking iron efflux from cells into plasma and reducing dietary iron absorption and release of stored iron[1][3][5][7]. Dysregulation of this pathway leads to pathologies such as iron overload (from hepcidin deficiency) or iron-restricted anemias (from hepcidin excess) and is implicated in chronic inflammation, infection, cancer, and immune modulation[4][8]. Pharmacological targeting of the hepcidin-ferroportin pathway involves inhibitors of hepcidin synthesis (e.g., targeting the BMP/SMAD or IL-6/STAT3 pathways), antibody-based therapies, and molecules modulating ferroportin stability[2][6]. Caveat: The *target* as written ("Hepcidin pathway") is not a single molecule but a regulatory pathway that includes peptide hormone (hepcidin), receptor/transporter (ferroportin), and upstream signaling components. For structured data, more granular entries for "Hepcidin" (gene product/hormone) and "Ferroportin" (receptor/transporter) may be appropriate. Mark as is_incorrect: true as per specification.

Other names

Hepcidin pathwayHepcidin axisHepcidin regulatory pathwayHepcidin-ferroportin axis

Inhibition of BMP/SMAD pathway to decrease hepcidin synthesis; Inhibition of IL-6/JAK-STAT3 signaling to reduce hepcidin secretion; Direct inhibition of hepcidin synthesis; Modulation of ferroportin stability to restore iron export