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正常铁稳态的分子机制。

Molecular mechanisms of normal iron homeostasis.

机构信息

Oregon Health & Science University, Portland, OR 97239, USA.

出版信息

Hematology Am Soc Hematol Educ Program. 2009:207-14. doi: 10.1182/asheducation-2009.1.207.

DOI:10.1182/asheducation-2009.1.207
PMID:20008200
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5831338/
Abstract

Humans possess elegant control mechanisms to maintain iron homeostasis by coordinately regulating iron absorption, iron recycling, and mobilization of stored iron. Dietary iron absorption is regulated locally by hypoxia inducible factor (HIF) signaling and iron-regulatory proteins (IRPs) in enterocytes and systematically by hepatic hepcidin, the central iron regulatory hormone. Hepcidin not only controls the rate of iron absorption but also determines iron mobilization from stores through negatively modulating the function of ferroportin, the only identified cellular iron exporter to date. The regulation of hepatic hepcidin is accomplished by the coordinated activity of multiple proteins through different signaling pathways. Recent studies have greatly expanded the knowledge in the understanding of hepcidin expression and regulation by the bone morphogenetic protein (BMP) signaling, the erythroid factors, and inflammation. In this review, we mainly focus on the roles of recently identified proteins in the regulation of iron homeostasis.

摘要

人类通过协调调节铁吸收、铁循环和储存铁的动员,拥有优雅的控制机制来维持铁平衡。肠道细胞中的缺氧诱导因子 (HIF) 信号和铁调节蛋白 (IRP) 局部调节膳食铁吸收,而肝脏中的亚铁肽作为中央铁调节激素系统地调节铁吸收。亚铁肽不仅控制铁吸收的速度,还通过负调控目前唯一鉴定出的细胞铁输出蛋白——亚铁转运蛋白的功能来决定铁从储存中的动员。肝脏亚铁肽的调节是通过多种蛋白质通过不同的信号通路的协调活动来实现的。最近的研究极大地扩展了人们对骨形态发生蛋白 (BMP) 信号、红细胞因子和炎症对亚铁肽表达和调节的认识。在这篇综述中,我们主要关注最近发现的在调节铁平衡中起作用的蛋白质。

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本文引用的文献

1
A ferroportin transcript that lacks an iron-responsive element enables duodenal and erythroid precursor cells to evade translational repression.一种缺乏铁反应元件的铁转运蛋白转录本使十二指肠和红系前体细胞能够逃避翻译抑制。
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Lack of the bone morphogenetic protein BMP6 induces massive iron overload.骨形态发生蛋白BMP6的缺失会导致大量铁过载。
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9
BMP6 is a key endogenous regulator of hepcidin expression and iron metabolism.骨形态发生蛋白6是铁调素表达和铁代谢的关键内源性调节因子。
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Hepcidin-induced internalization of ferroportin requires binding and cooperative interaction with Jak2.铁调素诱导的铁转运蛋白内化需要与Jak2结合并协同相互作用。
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