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Tumor necrosis factor alpha has an early protective effect on retinal ganglion cells after optic nerve crush

机译:肿瘤坏死因子α对视神经压伤后的视网膜神经节细胞具有早期保护作用

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摘要

BackgroundGlaucoma is an optic neuropathy that is characterized by the loss of retinal ganglion cells (RGCs) initiated by damage to axons in the optic nerve. The degeneration and death of RGCs has been thought to occur in two waves. The first is axogenic, caused by direct insult to the axon. The second is somatic, and is thought to be caused by the production of inflammatory cytokines from the activated retinal innate immune cells. One of the cytokines consistently linked to glaucoma and RGC damage has been TNFα. Despite strong evidence implicating this protein in neurodegeneration, a direct injection of TNFα does not mimic the rapid loss of RGCs observed after acute optic nerve trauma or exposure to excitotoxins. This suggests that our understanding of TNFα signaling is incomplete.
机译:背景技术青光眼是一种视神经病,其特征在于视神经中轴突的损伤引发视网膜神经节细胞(RGC)的丧失。人们认为RGC的退化和死亡发生在两次浪潮中。第一种是轴突生成,是由对轴突的直接侮辱引起的。第二种是体细胞的,被认为是由活化的视网膜先天免疫细胞产生炎性细胞因子引起的。与青光眼和RGC损伤始终相关的细胞因子之一是TNFα。尽管有强有力的证据表明该蛋白参与神经退行性变,但直接注射TNFα并不能模拟在急性视神经损伤或暴露于兴奋性毒素后观察到的RGC的快速丧失。这表明我们对TNFα信号的理解是不完整的。

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