内皮细胞Cdk5缺陷通过CXCL1/ cxcr2介导的反应性星形胶质细胞形成导致自发性癫痫的发生

Xiuxiu Liu, Lin Yang, Ling-Xiao Shao, Yang He, Gang Wu, Y. Bao, Nan-nan Lu, Dong-Mei Gong, Yangyang Lu, Tian-Tian Cui, Ninghe Sun, Dan-yang Chen, W. Shi, K. Fukunaga, Hong-Shan Chen, Zhong Chen, Feng Han, Ying-Mei Lu
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引用次数: 32

摘要

Liu等人揭示了脑血管损伤向癫痫转变的关键机制。他们发现内皮细胞周期蛋白依赖性激酶5 (CDK5)通过CXCL1/ cxcr2介导的星形胶质细胞形成调节星形细胞谷氨酸再摄取和谷氨酸突触功能增加。
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Endothelial Cdk5 deficit leads to the development of spontaneous epilepsy through CXCL1/CXCR2-mediated reactive astrogliosis
Liu et al. reveal a key mechanism that mediating the transition from cerebrovascular damage to epilepsy. They identify the endothelial cyclin-dependent kinase 5 (CDK5) regulates astrocytic glutamate reuptake and increased glutamate synaptic function through CXCL1/CXCR2-mediated astrogliosis.
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