期刊
BLOOD
卷 120, 期 9, 页码 1916-1922出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2012-04-423715
关键词
-
类别
资金
- National Institutes of Health
- Howard Hughes Medical Institute
- Alnylam Inc.
Anemia linked to a relative deficiency of renal erythropoietin production is a significant cause of morbidity and medical expenditures in the developed world. Recombinant erythropoietin is expensive and has been linked to excess cardiovascular events. Moreover, some patients become refractory to erythropoietin because of increased production of factors such as hepcidin. During fetal life, the liver, rather than the kidney, is the major source of erythropoietin. In the present study, we show that it is feasible to reactivate hepatic erythropoietin production and suppress hepcidin levels using systemically delivered siRNAs targeting the EglN prolyl hydroxylases specifically in the liver, leading to improved RBC production in models of anemia caused by either renal insufficiency or chronic inflammation with enhanced hepcidin production. (Blood. 2012;120(9):1916-1922)
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