Recycling Iron in Normal and Pathological States
Recycling Iron in Normal and Pathological States
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DOI：
10.1053/j.seminhematol.2009.06.004
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发表时间：
2009-10-01
影响因子：
3.6
通讯作者：
Delaby, Constance
中科院分区：
文献类型：
--
作者：
Beaumont, Carole;Delaby, Constance
在过去的10年里，我们对铁代谢的理解取得了重要的进展，强调了铁稳态失调导致血液、代谢和神经退行性疾病的机制。特别是，hepcidin的发现及其作为调节铁代谢的激素肽的基本作用，描绘了调节体内铁代谢的复杂蛋白质网络的组织。铁稳态的维持是肠细胞从饮食中吸收铁和衰老红细胞降解后巨噬细胞再循环铁之间紧密协调的结果。因此，这些过程的任何扰动都会导致广泛的疾病，从缺铁性贫血到铁超载。本文将重点讨论巨噬细胞铁循环的机制，并总结影响这一过程的病理条件。半血液学46:28 -338。(C) 2009爱思唯尔公司版权所有。
Important advances in our understanding of iron metabolism have been made during the past 10 years, highlighting the mechanisms by which dysregulated iron homeostasis leads to hematologic, metabolic, and neurodegenerative diseases. In particular, the discovery of hepcidin and its fundamental role as the hormonal peptide regulating iron metabolism has delineated the organization of the complex network of proteins that regulates iron metabolism within the body. Maintenance of iron homeostasis is the consequence of tight coordination between iron absorption from the diet by enterocytes, and iron recycling by macrophages following degradation of senescent erythrocytes. Thus, any perturbation of these processes leads to a wide spectrum of diseases, ranging from iron deficiency anemia to iron overload. This review will focus particularly on the mechanisms involved in iron recycling by macrophages and summarize the pathological conditions perturbing this process. Semin Hematol 46:328-338. (C) 2009 Elsevier Inc. All rights reserved.