摘要
铁是所有生物所需的基本元素,但它也可以产生有毒的氧化剂。因此,哺乳动物体内铁的稳态受到了严格的调节。铁调素25(hepcidin)已经成为一个调控铁代谢的分子。结合铁调素及其受体、膜铁转运蛋白可抑制肠道铁的吸收和来自肝细胞和巨噬细胞的铁流失,而抑制铁调素可提高铁的吸收和外排。铁调素可以预测铁状态和对补充铁剂或促红细胞生成素刺激剂作出反应,因此检测铁调素有助于对贫血进行处理。因此,获得一大群健康受试者的正常参考值和规范各类铁调素的检测是当务之急,这些数据可以比较不同的方法测得。贫血是一个与慢性肾脏疾病(CKD)紧密联系的重要而又常见的问题,通常由促红细胞生成素缺乏、缺铁性红细胞生成、炎症、缺氧、维生素D缺乏、甲状旁腺功能亢进、肥胖等病症引起的。贫血导致生活质量下降,慢性肾脏疾病发生,心血管疾病风险增加,死亡率增加。除了它在贫血中的作用外,最近的证据表明,铁调素25在调节铁介导的肾脏氧化损伤的发病机制及其进展中发挥着重要的作用。除了目前正在收集的实验数据,对CKD患者贫血和肾脏损伤的铁调素25的临床意义相关的信息仍然稀缺,尤其是儿童。本文综述了在成人和儿童CKD患者中铁调素25对贫血和肾脏损伤调节作用的当前的信息,并探讨怎样通过调节铁调素25防止CKD患者进一步贫血和肾脏损伤的一些策略。
关键词: 贫血,红细胞,铁蛋白,铁调素25,缺氧,炎症,铁,肾损伤。
Current Medicinal Chemistry
Title:Role of Hepcidin-25 in Chronic Kidney Disease: Anemia and Beyond
Volume: 24 Issue: 14
关键词: 贫血,红细胞,铁蛋白,铁调素25,缺氧,炎症,铁,肾损伤。
摘要: Iron is an essential element for all living organisms, but produces toxic oxidants. Thus, iron homeostasis is tightly regulated in mammals. Hepcidin-25 (hepcidin) has emerged as a molecule that regulates iron metabolism. Binding of hepcidin to its receptor, ferroportin, inhibits intestinal iron absorption and iron efflux from hepatocytes and macrophages. Decreased hepcidin enhances iron absorption and efflux. Hepcidin could be predictive of iron status and the response to iron supplementation or erythropoietin-stimulating agents. Monitoring hepcidin is helpful for the management of anemia. Thus, it is urgent to obtain normal reference values in a large population of healthy subjects and to standardize various hepcidin assays, which enables to compare the data measured by different methods. Anemia is an important and common problem associated with chronic kidney disease (CKD), which is caused by erythropoietin deficiency, iron-restricted erythropoiesis, inflammation, hypoxia, vitamin D deficiency, hyperparathyroidism, and obesity. Anemia causes poor quality of life, progression of CKD, increased risk of cardiovascular events, and mortality. Besides its role in anemia, recent evidence suggests that hepcidin-25 plays a role in the pathogenesis and progression of kidney injury via modulation of iron-mediated oxidant injury. Despite accumulating experimental data, information about clinical significance of hepcidin-25 for anemia and kidney injury in CKD patients is scarce, especially in children. This review summarizes the current knowledge of the role of hepcidin-25 in the regulation of anemia and kidney injury in children and adults with CKD. Strategy for modulating hepcidin-25 to prevent anemia and kidney injury associated with CKD is also discussed.
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Cite this article as:
Role of Hepcidin-25 in Chronic Kidney Disease: Anemia and Beyond, Current Medicinal Chemistry 2017; 24 (14) . https://dx.doi.org/10.2174/0929867324666170316120538
DOI https://dx.doi.org/10.2174/0929867324666170316120538 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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