Src Family Kinases in Brain Edema After Acute Brain Injury.
Src Family Kinases in Brain Edema After Acute Brain Injury.
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DOI：
10.1007/978-3-319-18497-5_33
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发表时间：
2016
期刊：
影响因子：
--
通讯作者：
Ander, Bradley P
中科院分区：
文献类型：
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作者：
Liu, DaZhi;Zhang, Xiong;Hu, BeiLei;Ander, Bradley P
脑水肿是颅内高压的第一阶段，与急性脑损伤（如缺血性卒中、颅内出血（ICH）和创伤性脑损伤（TBI））后的不良预后和死亡率增加相关。急性脑损伤通常引发许多分子的释放，包括谷氨酸、腺苷、凝血酶、氧合血红蛋白、细胞因子、活性氧（ROS）、损伤相关分子模式分子（DAMP）等。这些分子中的大多数激活Src家族激酶（SFKs），一种原癌非受体酪氨酸激酶家族，导致脑损伤后急性期血脑屏障（BBB）破坏和脑水肿。然而，SFKs也有助于脑损伤后慢性阶段的BBB自我修复和脑水肿消退。在这篇综述中，我们总结了SFKs参与脑水肿形成及其最终解决的可能途径。
Brain edema, the first stage of intracranial hypertension, has been associated with poor prognosis and increased mortality after acute brain injury, such as ischemic stroke, intracranial hemorrhage (ICH), and traumatic brain injury (TBI). The acute brain injury often initiates release of many molecules, including glutamate, adenosine, thrombin, oxyhemoglobin, cytokines, reactive oxygen species (ROS), damage associated molecular pattern molecules (DAMPs), and others. Most of those molecules activate Src family kinases (SFKs), a family of proto-oncogenic non-receptor tyrosine kinases, resulting in blood-brain barrier (BBB) disruption and brain edema at the acute stage after brain injury. However, SFKs also contributes to BBB self-repair and brain edema resolution in the chronic stage that follows brain injury. In this review we summarize possible pathways through which SFKs are implicated in both brain edema formation and its eventual resolution.