From the Guidelines

Hepcidin plays a crucial role in preventing iron overload by regulating iron homeostasis in the body.

Hepcidin is a 25-amino acid peptide hormone that binds to ferroportin, resulting in its internalization and degradation, thereby blocking cellular iron export 1.
This obstruction leads to a decrease in serum iron levels by blocking iron absorption from the intestine, iron recycling from macrophages, and mobilization of stored iron from liver hepatocytes 1.
Hepcidin expression is induced by excess iron or inflammation, resulting in decreased intestinal iron absorption and diminished iron release from macrophages 1.
Conversely, hepcidin expression is decreased by iron deficiency, ineffective erythropoiesis, and hypoxia, leading to increased iron absorption from the intestine and release of iron from macrophages 1.

Hepcidin synthesis is controlled by various physiologic and pathologic triggers, including circulating and stored iron levels, erythropoietic activity, hypoxia, and innate immune signaling 1.
Iron and inflammation induce hepcidin production, while iron deficiency and erythropoietic drive suppress it 1.
Hepcidin regulation is also influenced by other factors, such as erythropoietin, testosterone, and estrogen 1.

Dysregulation of hepcidin plays a key role in the pathogenesis of hemochromatosis and other iron overload disorders 1.
Measurement of hepcidin levels may be useful in screening, monitoring, and managing iron overload conditions, as well as in diagnosing and treating iron deficiency anemia 1.

From the Research

Hepcidin is the central regulator of iron homeostasis in the body, and its production is stimulated by inflammation or iron overload 2.
Mutations in the human haemochromatosis (HFE) gene can lead to a deficiency of hepcidin, resulting in iron overload and contributing to haemochromatosis 2, 3, 4.
Hepcidin plays a key role in regulating systematic iron homeostasis, controlling dietary iron absorption and iron egress out of iron storage cells, and inducing iron redistribution in various organs 3.
In iron overload disorders, such as hereditary hemochromatosis and β-thalassemia, hepatic hepcidin concentration is significantly reduced 3, 4.
Elevating hepcidin concentration is an optimal strategy to ameliorate iron overload diseases, and therapeutics targeting hepcidin could open a new avenue for treatment of iron-related diseases 3.
Hepcidin deficiency has been reported in various genetic causes of iron overload, including thalassemia syndromes and congenital dyserythropoietic anemia type 1 4.
The hepcidin-ferroportin interaction is critical in iron homeostasis, and alterations in this interaction can result in dysregulated iron absorption and tissue maldistribution of iron 4, 5.