期刊
NATURE GENETICS
卷 46, 期 7, 页码 678-684出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ng.2996
关键词
-
资金
- US National Institutes of Health (NIH) [CA-16042, AI-28697]
- JCCC
- UCLA AIDS Institute
- David Geffen School of Medicine at UCLA
- JCCC from US NIH [P30-CA-016042]
- CURE: Digestive Disease Research Core Center from US NIH [P30-DK-041301]
- US NIH [R01-DK-065029]
- American Society of Hematology scholar award
- [R01-DK-090554]
- [5R01-DK-095112]
Recovery from blood loss requires a greatly enhanced supply of iron to support expanded erythropoiesis. After hemorrhage, suppression of the iron-regulatory hormone hepcidin allows increased iron absorption and mobilization from stores. We identified a new hormone, erythroferrone (ERFE), that mediates hepcidin suppression during stress erythropoiesis. ERFE is produced by erythroblasts in response to erythropoietin. ERFE-deficient mice fail to suppress hepcidin rapidly after hemorrhage and exhibit a delay in recovery from blood loss. ERFE expression is greatly increased in Hbb(th3/+) mice with thalassemia intermedia, where it contributes to the suppression of hepcidin and the systemic iron overload characteristic of this disease.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据