Ironing out Ferroportin

被引:609
作者
Drakesmith, Hal [1 ]
Nemeth, Elizabeta [2 ]
Ganz, Tomas [2 ,3 ]
机构
[1] Univ Oxford, Weatherall Inst Mol Med, MRC Human Immunol Unit, Oxford OX3 9DS, England
[2] Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Los Angeles, CA 90095 USA
[3] Univ Calif Los Angeles, David Geffen Sch Med, Dept Pathol, Los Angeles, CA 90095 USA
基金
美国国家卫生研究院; 英国医学研究理事会;
关键词
SERUM FERRITIN; MONOCYTE DIFFERENTIATION; TYPHIMURIUM INFECTION; FERROXIDASE ACTIVITY; MOLECULAR-MECHANISM; MEDIATED REGULATION; RESPONSIVE ELEMENT; AFRICAN-AMERICANS; MOUSE MODEL; IN-VITRO;
D O I
10.1016/j.cmet.2015.09.006
中图分类号
Q2 [细胞生物学];
学科分类号
071013 [干细胞生物学];
摘要
Maintaining physiologic iron concentrations in tissues is critical for metabolism and host defense. Iron absorption in the duodenum, recycling of iron from senescent erythrocytes, and iron mobilization from storage in macrophages and hepatocytes constitute the major iron flows into plasma for distribution to tissues, predominantly for erythropoiesis. All iron transfer to plasma occurs through the iron exporter ferroportin. The concentration of functional membrane-associated ferroportin is controlled by its ligand, the iron-regulatory hormone hepcidin, and fine-tuned by regulatory mechanisms serving iron homeostasis, oxygen utilization, host defense, and erythropoiesis. Fundamental questions about the structure and biology of ferroportin remain to be answered.
引用
收藏
页码:777 / 787
页数:11
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