A role for calpain in optic neuritis
A role for calpain in optic neuritis
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DOI：
10.1196/annals.1344.005
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发表时间：
2005-01-01
期刊：
影响因子：
--
通讯作者：
Banik, NL
中科院分区：
文献类型：
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作者：
Guyton, MK;Sribnick, EA;Banik, NL
视神经炎（ON）是多发性硬化症（MS）最常见的症状之一，多发性硬化症是中枢神经系统（CNS）的神经退行性疾病，被认为是由自身反应性T细胞和其他免疫细胞对髓鞘的攻击引起的。实验性自身免疫性脑脊髓炎（EAE）是MS和ON的广泛使用的模型，其特征在于脱髓鞘、轴突损伤和神经元死亡。神经变性的机制尚不清楚;然而，钙（Ca 2+）依赖性中性蛋白酶钙蛋白酶被认为参与其中。本文的重点是总结证据表明，钙蛋白酶在刘易斯大鼠EAE-ON的发展中发挥作用。
Optic neuritis (ON) is one of the most commonly presenting symptoms of multiple sclerosis (MS), which is a neurodegenerative disease of the central nervous system (CNS) thought to be caused by an attack on myelin by autoreactive T cells and other immune cells. Experimental autoimmune encephalomyelitis (EAE) is a widely used model for MS and ON, which are characterized by demyelination, axonal damage, and neuronal death. The mechanisms of neurodegeneration are unclear; however, the calcium (Ca2+)dependent neutral protease calpain is thought to be involved. The focus of this article is to summarize the evidence suggesting that calpain plays a role in the development of EAE-ON in Lewis rats.