Hepcidin-Ferroportin Interaction Controls Systemic Iron Homeostasis.
Hepcidin-Ferroportin Interaction Controls Systemic Iron Homeostasis.
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DOI:
10.3390/ijms22126493
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发表时间:
2021-06-17
影响因子:
5.6
通讯作者:
Ganz T
中科院分区:
文献类型:
--
作者:
Nemeth E;Ganz T
Despite its abundance in the environment, iron is poorly bioavailable and subject to strict conservation and internal recycling by most organisms. In vertebrates, the stability of iron concentration in plasma and extracellular fluid, and the total body iron content are maintained by the interaction of the iron-regulatory peptide hormone hepcidin with its receptor and cellular iron exporter ferroportin (SLC40a1). Ferroportin exports iron from duodenal enterocytes that absorb dietary iron, from iron-recycling macrophages in the spleen and the liver, and from iron-storing hepatocytes. Hepcidin blocks iron export through ferroportin, causing hypoferremia. During iron deficiency or after hemorrhage, hepcidin decreases to allow iron delivery to plasma through ferroportin, thus promoting compensatory erythropoiesis. As a host defense mediator, hepcidin increases in response to infection and inflammation, blocking iron delivery through ferroportin to blood plasma, thus limiting iron availability to invading microbes. Genetic diseases that decrease hepcidin synthesis or disrupt hepcidin binding to ferroportin cause the iron overload disorder hereditary hemochromatosis. The opposite phenotype, iron restriction or iron deficiency, can result from genetic or inflammatory overproduction of hepcidin.
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影响因子:
30.3
作者:
Arezes J;Jung G;Gabayan V;Valore E;Ruchala P;Gulig PA;Ganz T;Nemeth E;Bulut Y
通讯作者:
Bulut Y
影响因子:
20.3
作者:
Jiang L;Wang J;Wang K;Wang H;Wu Q;Yang C;Yu Y;Ni P;Zhong Y;Song Z;Xie E;Hu R;Min J;Wang F
通讯作者:
Wang F
影响因子:
3.6
作者:
Beaumont, Carole;Delaby, Constance
通讯作者:
Delaby, Constance
影响因子:
20.3
作者:
Ganz, Tomas;Olbina, Gordana;Westerman, Mark
通讯作者:
Westerman, Mark
影响因子:
6
作者:
Jiang, Shuxia;Fang, Xi;Zhao, Ruqian
通讯作者:
Zhao, Ruqian