Endothelial Cdk5 deficit leads to the development of spontaneous epilepsy through CXCL1/CXCR2-mediated reactive astrogliosis
Endothelial Cdk5 deficit leads to the development of spontaneous epilepsy through CXCL1/CXCR2-mediated reactive astrogliosis
复制标题
内皮 Cdk5 缺陷通过 CXCL1/CXCR2 介导的反应性星形胶质细胞增生导致自发性癫痫的发生
DOI：
10.1084/jem.20180992
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发表时间：
2020-01-01
影响因子：
15.3
通讯作者：
Lu, Ying-mei
中科院分区：
文献类型：
--
作者：
Liu, Xiu-xiu;Yang, Lin;Lu, Ying-mei
Liu等揭示了介导脑血管损伤向癫痫转变的关键机制。他们确定了内皮细胞周期蛋白依赖性激酶5（CDK 5）通过CXCL 1/CXCR 2介导的星形胶质细胞增生调节星形胶质细胞谷氨酸再摄取和增加谷氨酸突触功能。
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.