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SP1-mediated upregulation of LINGO-1 promotes degeneration of retinal ganglion cells in optic nerve injury.
CNS Neuroscience & Therapeutics ( IF 4.8 ) Pub Date : 2020-06-19 , DOI: 10.1111/cns.13426
Yali Wu 1 , Zongyi Zhan 1 , Yadan Quan 1 , Yangfan Yang 1 , Xiaotao Chen 1 , Liling Liu 1 , Kaili Wu 1 , Minbin Yu 1
Affiliation  

Insults to the axons in the optic nerve head are the primary cause of loss of retinal ganglion cells (RGCs) in traumatic, ischemic nerve injury or degenerative ocular diseases. The central nervous system–specific leucine‐rich repeat protein, LINGO‐1, negatively regulates axon regeneration and neuronal survival after injury. However, the upstream molecular mechanisms that regulate LINGO‐1 signaling and contribute to LINGO‐1–mediated death of RGCs are unclear.

中文翻译:


SP1 介导的 LINGO-1 上调促进视神经损伤中视网膜神经节细胞的变性。



视神经乳头轴突的损伤是创伤性、缺血性神经损伤或退行性眼病中视网膜神经节细胞 (RGC) 损失的主要原因。中枢神经系统特异性富含亮氨酸的重复蛋白 LINGO-1 负向调节轴突再生和损伤后神经元存活。然而,调节 LINGO-1 信号传导并导致 LINGO-1 介导的 RGC 死亡的上游分子机制尚不清楚。
更新日期:2020-06-19
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