Iron regulation by hepcidin

J Clin Invest. 2013 Jun;123(6):2337-43. doi: 10.1172/JCI67225. Epub 2013 Jun 3.


Hepcidin is a key hormone that is involved in the control of iron homeostasis in the body. Physiologically, hepcidin is controlled by iron stores, inflammation, hypoxia, and erythropoiesis. The regulation of hepcidin expression by iron is a complex process that requires the coordination of multiple proteins, including hemojuvelin, bone morphogenetic protein 6 (BMP6), hereditary hemochromatosis protein, transferrin receptor 2, matriptase-2, neogenin, BMP receptors, and transferrin. Misregulation of hepcidin is found in many disease states, such as the anemia of chronic disease, iron refractory iron deficiency anemia, cancer, hereditary hemochromatosis, and ineffective erythropoiesis, such as β-thalassemia. Thus, the regulation of hepcidin is the subject of interest for the amelioration of the detrimental effects of either iron deficiency or overload.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antimicrobial Cationic Peptides / genetics
  • Antimicrobial Cationic Peptides / metabolism*
  • Bone Morphogenetic Proteins / metabolism
  • Cell Hypoxia
  • Chronic Disease
  • GPI-Linked Proteins / metabolism
  • Gene Expression Regulation
  • Hematopoiesis
  • Hemochromatosis Protein
  • Hepcidins
  • Humans
  • Iron / metabolism*
  • Matrix Metalloproteinase 15 / metabolism
  • Receptors, Transferrin / metabolism
  • Signal Transduction
  • beta-Thalassemia / blood
  • beta-Thalassemia / genetics


  • Antimicrobial Cationic Peptides
  • Bone Morphogenetic Proteins
  • GPI-Linked Proteins
  • HAMP protein, human
  • HJV protein, human
  • Hemochromatosis Protein
  • Hepcidins
  • Receptors, Transferrin
  • TFR2 protein, human
  • Iron
  • Matrix Metalloproteinase 15