Ganz Tomas
Departments of Medicine and Pathology, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
Isr Med Assoc J. 2002 Nov;4(11):1043-5.
Systemic infection or inflammation causes a decrease in intestinal iron absorption and impairs the release of recycled iron from macrophages. Decreased availability of iron may deny this essential element to invading pathogens and may inhibit their multiplication and other metabolic processes but also results in anemia of chronic disease. This article reviews recent discoveries that shed light on the regulation of iron metabolism during infection and iron overload, and point to the central role of a newly discovered peptide, hepcidin. Evidence to date indicates that hepcidin is a negative regulator of intestinal iron absorption, placental iron transport, and the release of iron from macrophages that recycle iron from senescent red cells. It may also be the central mediator of iron sequestration during infections and inflammatory states and the mediator of anemia of chronic disease. Rapid progress in this area is a good example of the beneficial effects of improvements in peptide analysis and chemistry, advances in genomics, and the increasing use of transgenic mice to determine the function of newly discovered genes and proteins.
全身感染或炎症会导致肠道铁吸收减少，并损害巨噬细胞中循环铁的释放。铁的可利用性降低可能会使入侵病原体无法获得这种必需元素，并可能抑制它们的繁殖和其他代谢过程，但也会导致慢性病贫血。本文综述了近期的一些发现，这些发现揭示了感染和铁过载期间铁代谢的调节机制，并指出了一种新发现的肽——铁调素的核心作用。迄今为止的证据表明，铁调素是肠道铁吸收、胎盘铁转运以及巨噬细胞（从衰老红细胞中回收铁）释放铁的负调节因子。它也可能是感染和炎症状态下铁螯合的核心介质以及慢性病贫血的介质。该领域的快速进展是肽分析和化学改进、基因组学进步以及越来越多地使用转基因小鼠来确定新发现基因和蛋白质功能所带来有益影响的一个很好例证。
