Mechanisms and therapies for acute CNS insults.
Mechanisms and therapies for acute CNS insults.
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急性中枢神经系统损伤的机制和治疗。
DOI：
10.1007/s11011-014-9585-5
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发表时间：
2015
影响因子：
3.6
通讯作者：
Zhao,Heng
中科院分区：
文献类型：
--
作者：
Vemuganti,Raghu;Zhao,Heng
中风、创伤性脑损伤(TBI)和脊髓损伤(SCI)等急性中枢神经系统损伤后的继发性脑损伤是多种协同机制共同作用的结果。这期特刊的目的是讨论其中一些途径和当前的实验性治疗方法，以帮助将急性中枢神经系统损伤后的神经功能障碍降至最低。转录因子已知在中风后的炎症、氧化应激和神经元死亡以及神经保护和可塑性中发挥重要作用。Yen等人。讨论锌指转录因子家族在中风后保护神经元和毛细血管中的作用。众所周知，脑部炎症会显著影响神经前体细胞的增殖。在这方面，王和金讨论了各种炎症分子在调节中风后神经发生中的作用。由于GABA是哺乳动物大脑中主要的抑制性神经递质，其功能障碍在继发性脑损伤中扮演着重要角色，Wu和Sun讨论了GABA在各种形式的急性中枢神经系统损伤中的潜在作用，包括中风和脑外伤。神经胶质细胞通过调节炎症反应，在保护和加重急性中枢神经系统损伤后神经元死亡中发挥重要作用。Kawbori和Yenari展示了小胶质细胞在调节中风后继发性脑损伤中的作用。Ziebell等人。探讨小胶质细胞在脑外伤后神经元损伤中的作用。此外，Muradashvili等人。讨论……的意义
Multiple synergistic mechanisms contribute to secondary brain damage following acute insults to CNS like stroke, traumatic brain injury (TBI) and spinal cord injury (SCI). The goal of this special issue is to discuss some of those pathways and the current experimental therapeutic approaches that help minimize the neurological dysfunction after acute CNS injuries.Transcription factors are known to play a significant role in inflammation, oxidative stress and neuronal death as well as neuroprotection and plasticity after stroke. Yin et al. discuss the role of the zinc finger family of transcription factors; Krüppel-like factors in protecting neurons and capillaries after stroke. Cerebral inflammation is known to significantly influence neural progenitor cell proliferation. In this regard, Wang and Jin discuss the role of various inflammatory molecules in modulating neurogenesis after stroke. As GABA is the major inhibitory neurotransmitter in the mammalian brain and its dysfunction plays a role in secondary brain damage, Wu and Sun discuss the potential role of GABA in various forms of acute CNS injuries, including stroke and TBI. Glial cells play important roles in protecting as well as exacerbating neuronal death after acute CNS insults by modulating inflammatory reactions. Kawabori and Yenari show the role of microglia in mediating secondary brain damage following stroke. Ziebell et al. discuss the potential of microglia in the neuronal damage afterTBI. Furthermore, Muradashvili et al. discuss the significance of