Hepcidin regulation in the anemia of inflammation.
Hepcidin regulation in the anemia of inflammation.
复制标题
炎症贫血中的肝素调节。
DOI：
10.1097/moh.0000000000000236
复制
发表时间：
2016-05
影响因子：
3.2
通讯作者：
Babitt JL
中科院分区：
文献类型：
--
作者：
Wang CY;Babitt JL
贫血在感染和其他炎症性疾病患者中很普遍。铁调节激素铁调素的诱导与炎症性贫血（AI）的发病机制有关。本文概述了最近的发现，了解铁调素及其受体ferroportin是如何调节的，它们如何有助于AI，以及这些知识如何有助于指导这种疾病的新的诊断和治疗策略。在许多AI模型中，IL 6是铁调素诱导的主要驱动因素，但SMAD 1/5/8途径也有贡献，可能是通过铁调素启动子处的激活素B和SMAD-STAT 3相互作用。Hepcidin在许多但不是所有形式的AI中具有重要的功能作用，尽管hepcidin独立机制也有贡献。在某些人群中，铁调素测定可能有助于铁或红细胞生成刺激剂靶向治疗，以使患者受益最多。靶向铁调素-膜铁转运蛋白轴的新疗法已在临床前和早期临床研究中显示出疗效。最近的研究证实了铁调素-铁转运蛋白轴在AI发展中的重要作用，但也强调了这种疾病的发病机制取决于基础疾病的多样性和复杂性。基于铁调素的诊断和治疗策略有望改善贫血治疗，但在这方面还需要更多的工作。
Anemia is prevalent in patients with infections and other inflammatory conditions. Induction of the iron regulatory hormone hepcidin has been implicated in the pathogenesis of anemia of inflammation (AI). This review outlines recent discoveries in understanding how hepcidin and its receptor ferroportin are regulated, how they contribute to AI, and how this knowledge may help guide new diagnostic and therapeutic strategies for this disease. IL6 is a primary driver for hepcidin induction in many models of AI, but the SMAD1/5/8 pathway also contributes, likely via Activin B and SMAD-STAT3 interactions at the hepcidin promoter. Hepcidin has an important functional role in many, but not all, forms of AI, although hepcidin-independent mechanisms also contribute. In certain populations, hepcidin assays may help target therapy with iron or erythropoiesis stimulating agents to patients who may benefit most. New therapies targeting the hepcidin-ferroportin axis have shown efficacy in pre-clinical and early clinical studies. Recent studies confirm an important role for the hepcidin-ferroportin axis in the development of AI, but also highlight the diverse and complex pathogenesis of this disorder depending on the underlying disease. Hepcidin-based diagnostic and therapeutic strategies offer promise to improve anemia treatment, but more work is needed in this area.