Hemojuvelin and bone morphogenetic protein (BMP) signaling in iron homeostasis

被引：83

作者：

Core, Amanda B. ^{[1
]}

Canali, Susanna ^{[1
]}

Babitt, Jodie L. ^{[1
]}

机构：

[1] Harvard Univ, Sch Med, Massachusetts Gen Hosp,Program Membrane Biol, Ctr Syst Biol,Div Nephrol,Program Anemia Signalin, Boston, MA USA

来源：

FRONTIERS IN PHARMACOLOGY | 2014年 / 5卷

关键词：

hemojuvelin; bone morphogenetic protein; hepcidin; iron; hemochromatosis; repulsive guidance molecule; REPULSIVE GUIDANCE MOLECULE; HEPATIC HEPCIDIN EXPRESSION; GENOME-WIDE ASSOCIATION; TRANSFERRIN RECEPTOR 2; JUVENILE HEMOCHROMATOSIS; REGULATORY PROTEIN; SOLUBLE HEMOJUVELIN; MATRIPTASE-2; TMPRSS6; DEFICIENCY ANEMIA; PEPTIDE HEPCIDIN;

D O I：

10.3389/fphar.2014.00104

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Mutations in hemojuvelin (HJV) are the most common cause of the juvenile-onset form of the iron overload disorder hereditary hemochromatosis. The discovery that HJV functions as a co-receptor for the bone morphogenetic protein (BMP) family of signaling molecules helped to identify this signaling pathway as a central regulator of the key iron hormone hepcidin in the control of systemic iron homeostasis. This review highlights recent work uncovering the mechanism of action of HJV and the BMP-SMAD signaling pathway in regulating hepcidin expression in the liver, as well as additional studies investigating possible extra-hepatic functions of HJV. This review also explores the interaction between HJV, the BMP-SMAD signaling pathway and other regulators of hepcidin expression in systemic iron balance.

引用

页数：9

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