Molecular mediators governing iron-copper interactions.

Molecular mediators governing iron-copper interactions.
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DOI:
10.1146/annurev-nutr-071812-161215
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发表时间:
2014
影响因子:
8.9
通讯作者:
Collins JF
Collins JF
中科院分区:
医学2区
文献类型:
--
作者:
Gulec S;Collins JF

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考虑到它们相似的生理化学性质,铁和铜的代谢相互交织是一个合乎逻辑的假设。事实上,铁-铜相互作用在世纪前就被首次记载,但迄今为止,一种对另一种的稳态作用尚未在分子水平上阐明。然而,最近的实验工作已经开始提供铜如何影响铁代谢的机制见解。在缺铁期间,在肠粘膜、肝脏和血液中观察到铜水平升高。铜的积累和/或肠上皮细胞内的再分布可能会影响铁的转运,高肝铜可能会增强循环铁氧化酶的生物合成,从而增强铁从储存中的释放。此外,新出现的证据已经记录了铜对铁调节激素铁调素的表达和活性的直接影响。这篇综述总结了目前在这一领域的实验工作,重点是铁铜相互作用的分子方面,以及这些相互作用如何与各种疾病状态。
Given their similar physiochemical properties, it is a logical postulate that iron and copper metabolism are intertwined. Indeed, iron-copper interactions were first documented over a century ago, but the homeostatic effects of one on the other has not been elucidated at a molecular level to date. Recent experimental work has, however, begun to provide mechanistic insight into how copper influences iron metabolism. During iron deficiency, elevated copper levels are observed in the intestinal mucosa, liver, and blood. Copper accumulation and/or redistribution within enterocytes may influence iron transport, and high hepatic copper may enhance biosynthesis of a circulating ferroxidase, which potentiates iron release from stores. Moreover, emerging evidence has documented direct effects of copper on the expression and activity of the iron-regulatory hormone hepcidin. This review summarizes current experimental work in this field, with a focus on molecular aspects of iron-copper interplay and how these interactions relate to various disease states.
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