title: Regulation of Iron Metabolism by Hepcidin under Conditions of Inflammation.
abstract: Iron is a redox-active metal required as a cofactor in multiple metalloproteins essential for a host of life processes. The metal is highly toxic when present in excess and must be strictly regulated to prevent tissue and organ damage. Hepcidin, a molecule first characterized as an antimicrobial peptide, plays a critical role in the regulation of iron homeostasis. Multiple stimuli positively influence the expression of hepcidin, including iron, inflammation, and infection by pathogens. In this Minireview, I will discuss how inflammation regulates hepcidin transcription, allowing for sufficient concentrations of iron for organismal needs while sequestering the metal from infectious pathogens.
authors.affiliation: From the Department of Pathology, Boston Children's Hospital and Harvard Medical School, Boston, Massachusetts 02115 paul.schmidt@childrens.harvard.edu.
authors.forename: Paul J
authors.initials: PJ
authors.lastname: Schmidt
mesh_terms: D000818:Animals; D001424:Bacterial Infections / Q000276:immunology / Q000378:metabolism; D064451:Hepcidins / Q000502:physiology*; D006706:Homeostasis; D006801:Humans; D007113:Immunity, Innate; D007249:Inflammation / Q000378:metabolism; D007501:Iron / Q000378:metabolism*; D014777:Virus Diseases / Q000276:immunology / Q000378:metabolism
chemical_list: D064451:Hepcidins; D007501:Iron
keywords: STAT3; bone morphogenetic protein (BMP); cell signaling; hepcidin; infectious disease; inflammation; iron metabolism