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铁的摄入。IV. 铁调素与机体铁代谢的调节。

Iron imports. IV. Hepcidin and regulation of body iron metabolism.

作者信息

Ganz Tomas, Nemeth Elizabeta

机构信息

Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90095-1690, USA.

出版信息

Am J Physiol Gastrointest Liver Physiol. 2006 Feb;290(2):G199-203. doi: 10.1152/ajpgi.00412.2005.

Abstract

Hepcidin, a small peptide synthesized in the liver, controls extracellular iron by regulating its intestinal absorption, placental transport, recycling by macrophages, and release from stores. Hepcidin inhibits the cellular efflux of iron by binding to and inducing the degradation of ferroportin, the sole iron exporter in iron-transporting cells. In turn, hepcidin synthesis is increased by iron loading and decreased by anemia and hypoxia. Hepcidin is markedly induced during inflammation, trapping iron in macrophages, decreasing plasma iron concentrations, and contributing to the anemia of inflammation. Hepcidin deficiency due to the dysregulation of its synthesis causes most known forms of hemochromatosis.

摘要

铁调素是一种在肝脏中合成的小肽,它通过调节铁的肠道吸收、胎盘转运、巨噬细胞的再循环以及从储存部位的释放来控制细胞外铁。铁调素通过与铁转运蛋白(铁转运细胞中唯一的铁输出蛋白)结合并诱导其降解,从而抑制铁的细胞外排。反过来,铁负荷会增加铁调素的合成,而贫血和缺氧则会使其合成减少。在炎症期间,铁调素会显著诱导产生,将铁困在巨噬细胞中,降低血浆铁浓度,并导致炎症性贫血。由于铁调素合成失调导致的铁调素缺乏会引发大多数已知形式的血色素沉着症。

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