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本文引用的文献

1
Non-transferrin bound iron: a key role in iron overload and iron toxicity.非转铁蛋白结合铁:在铁过载和铁毒性中起关键作用。
Biochim Biophys Acta. 2012 Mar;1820(3):403-10. doi: 10.1016/j.bbagen.2011.07.014. Epub 2011 Aug 9.
2
Investigation of a researcher's death due to septicemic plague.一名研究人员因败血性鼠疫死亡的调查。
N Engl J Med. 2011 Jun 30;364(26):2563-4. doi: 10.1056/NEJMc1010939.
3
Mechanism for phosphatidylserine-dependent erythrophagocytosis in mouse liver.小鼠肝脏中依赖磷脂酰丝氨酸的红细胞吞噬作用的机制。
Blood. 2011 May 12;117(19):5215-23. doi: 10.1182/blood-2010-10-313239. Epub 2011 Mar 22.
4
Extracellular hemoglobin polarizes the macrophage proteome toward Hb-clearance, enhanced antioxidant capacity and suppressed HLA class 2 expression.细胞外血红蛋白使巨噬细胞蛋白质组向血红蛋白清除、增强抗氧化能力和抑制 HLA Ⅱ类表达极化。
J Proteome Res. 2011 May 6;10(5):2397-408. doi: 10.1021/pr101230y. Epub 2011 Apr 14.
5
An unrestrained proinflammatory M1 macrophage population induced by iron impairs wound healing in humans and mice.铁诱导的不受限制的促炎 M1 巨噬细胞群体会损害人类和小鼠的伤口愈合。
J Clin Invest. 2011 Mar;121(3):985-97. doi: 10.1172/JCI44490. Epub 2011 Feb 7.
6
Human heme oxygenase-1 deficiency presenting with hemolysis, nephritis, and asplenia.人类血红素加氧酶-1缺乏症表现为溶血、肾炎和无脾。
J Pediatr Hematol Oncol. 2011 Jan;33(1):74-8. doi: 10.1097/MPH.0b013e3181fd2aae.
7
Control of iron homeostasis as a key component of macrophage polarization.铁稳态的调控作为巨噬细胞极化的关键组成部分。
Haematologica. 2010 Nov;95(11):1801-3. doi: 10.3324/haematol.2010.030239.
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Hepcidin and disorders of iron metabolism.亚铁调素与铁代谢紊乱。
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The pathogenesis of Plasmodium falciparum malaria in humans: insights from splenic physiology.人类恶性疟原虫疟疾的发病机制:脾脏生理学的新见解。
Blood. 2011 Jan 13;117(2):381-92. doi: 10.1182/blood-2010-04-202911. Epub 2010 Sep 17.
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Dysfunction of the heme recycling system in heme oxygenase 1-deficient mice: effects on macrophage viability and tissue iron distribution.血红素氧合酶 1 缺陷小鼠血红素回收系统功能障碍:对巨噬细胞活力和组织铁分布的影响。
Blood. 2010 Dec 23;116(26):6054-62. doi: 10.1182/blood-2010-03-272138. Epub 2010 Sep 15.

巨噬细胞与全身铁稳态。

Macrophages and systemic iron homeostasis.

机构信息

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

出版信息

J Innate Immun. 2012;4(5-6):446-53. doi: 10.1159/000336423. Epub 2012 Mar 21.

DOI:10.1159/000336423
PMID:22441209
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6741611/
Abstract

As a principal aspect of their scavenging function, splenic and hepatic macrophages phagocytize and degrade senescent and damaged erythrocytes to recover iron, mainly for the production of hemoglobin in new erythrocytes but also for other carriers and enzymes requiring iron. Splenic red pulp macrophages are specialized for iron recycling with increased expression of proteins for the uptake of hemoglobin, breakdown of heme and the export of iron. In humans, recycling macrophages contribute the majority of the iron flux into extracellular fluid, exceeding the contribution of dietary iron absorption and release of stored iron from hepatocytes. Iron release from macrophages is closely regulated by the interaction of hepcidin, a peptide hormone produced by hepatocytes, with the macrophage iron exporter ferroportin. In addition to their homeostatic role, macrophages employ multiple mechanisms to contain microbial infections by depriving microbes of iron. This review discusses the iron-scavenging function of macrophages in the context of iron homeostasis and host defense.

摘要

作为其清除功能的主要方面,脾和肝巨噬细胞吞噬和降解衰老和受损的红细胞以回收铁,主要用于新红细胞的血红蛋白生成,但也用于其他需要铁的载体和酶。脾红髓巨噬细胞专门用于铁的再循环,其摄取血红蛋白、分解血红素和输出铁的蛋白表达增加。在人类中,再循环巨噬细胞对细胞外液中铁通量的贡献最大,超过了膳食铁吸收和肝细胞储存铁释放的贡献。巨噬细胞中铁的释放受到由肝细胞产生的肽激素——铁调素与巨噬细胞铁输出蛋白 Ferroportin 相互作用的密切调节。除了其维持体内平衡的作用外,巨噬细胞还通过剥夺微生物的铁来利用多种机制来控制微生物感染。本综述讨论了巨噬细胞在铁稳态和宿主防御中的铁清除功能。