The role of iron in the pathogenesis of experimental allergic encephalomyelitis and multiple sclerosis
The role of iron in the pathogenesis of experimental allergic encephalomyelitis and multiple sclerosis
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DOI：
10.1196/annals.1306.021
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发表时间：
2004-01-01
期刊：
影响因子：
--
通讯作者：
Chakrabarty, A
中科院分区：
文献类型：
--
作者：
LeVine, SM;Chakrabarty, A
多发性硬化（MS）及其动物模型实验性变态反应性脑脊髓炎（EAE）是导致中枢神经系统（CNS）脱髓鞘的自身免疫性疾病。病理学上，血脑屏障受损，巨噬细胞和T细胞进入CNS，少突胶质细胞和髓鞘被破坏，星形胶质细胞和小胶质细胞发生神经胶质增生，轴突被切断。一些生物化学和药理学研究的数据表明，自由基参与EAE的发病机制，铁被认为是导致其形成的催化剂。本文的主要重点是铁在MS和EAE发病机制中的作用。将特别注意铁和与铁代谢有关的蛋白质的作用和分布（例如，转铁蛋白、铁蛋白、血红素加氧酶-1等）在髓鞘的正常和疾病状态下。此外，针对铁，铁结合蛋白，和铁催化反应的底物或产物，导致自由基的产生的治疗干预措施将进行讨论。
Multiple sclerosis (MS) and its animal model, experimental allergic encephalomyelitis (EAE), are autoimmune disorders resulting in demyelination in the central nervous system (CNS). Pathologically, the blood-brain barrier becomes damaged, macrophages and T cells enter into the CNS, oligodendrocytes and myelin are destroyed, astrocytes and microglia undergo gliosis, and axons become transected. Data from several biochemical and pharmacological studies indicate that free radicals participate in the pathogenesis of EAE, and iron has been implicated as the catalyst leading to their formation. The primary focus of this article is the examination of the role of iron in the pathogenesis of MS and EAE. Particular attention will be paid to the role and distribution of iron and proteins involved with iron metabolism (e.g., transferrin, ferritin, heme oxygenase-1, etc.) in normal and disease states of myelin. Furthermore, therapeutic interventions aimed at iron, iron-binding proteins, and substrates or products of iron-catalyzed reactions leading to free radical production will be discussed.