Iron regulation by hepcidin

• Published in: The Journal of clinical investigation Vol. 123; no. 6; pp. 2337 - 2343
• Main Authors: Zhao, Ningning, Zhang, An-Sheng, Enns, Caroline A.
• Format: Journal Article
• Language: English
• Published: United States American Society for Clinical Investigation 01.06.2013
• Subjects: Animals; Antimicrobial Cationic Peptides - genetics; Antimicrobial Cationic Peptides - metabolism; beta-Thalassemia - blood; beta-Thalassemia - genetics; Biomedical research; Bone Morphogenetic Proteins - metabolism; Cell Hypoxia; Chronic Disease; Control; Gene Expression Regulation; GPI-Linked Proteins - metabolism; Hematopoiesis; Hepcidins; Homeostasis; Humans; Identification and classification; Iron - metabolism; Iron in the body; Kinases; Matrix Metalloproteinase 15 - metabolism; Mutation; Peptide hormones; Physiological aspects; Properties; Proteins; Receptors, Transferrin - metabolism; Rodents; Science in Medicine; Signal Transduction
• ISSN: 0021-9738; 1558-8238; 1558-8238
• DOI: 10.1172/JCI67225

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.