NF-κB and innate immunity in ischemic stroke.
NF-κB and innate immunity in ischemic stroke.
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DOI：
10.1111/j.1749-6632.2010.05735.x
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发表时间：
2010-10
影响因子：
5.2
通讯作者：
Liao JK
中科院分区：
文献类型：
--
作者：
Harari OA;Liao JK
急性脑缺血引发先天性免疫反应，导致一系列事件，最终导致神经元坏死死亡和神经血管单位中支持结构的损伤。事实上，临床研究已经表明炎症标志物水平升高与缺血性卒中风险之间存在密切关系。然而，连接这些事件的信号通路并不清楚。炎症反应的中心调节因子是转录因子核因子-κ B（NF-κB）。NF-κB的活化是先天免疫中涉及的许多促炎介质（如细胞粘附分子、细胞因子和生长因子）的转录诱导所必需的。因此，NF-κB活性调节因子可能在缺血性卒中中调节炎症过程。在此，我们综述了NF-κB与缺血性卒中的关系，它在神经血管单位中的作用，并讨论了一些动物模型，表明这种关系是因果关系。
Acute cerebral ischemia elicits an innate immune response that leads to a cascade of events that culminates in necrotic death of neurons and injury to their supportive structures in the neurovascular unit. Indeed, clinical studies have shown a close relationship between elevated levels of inflammatory markers and the risk for ischemic stroke. However, the signaling pathways that link these events are not well understood. A central regulator of inflammatory response is the transcription factor, nuclear factor-kappa B (NF-κB). The activation of NF-κB is required for the transcriptional induction of many proinflammatory mediators involved in innate immunity, such as cellular adhesion molecules, cytokines, and growth factors. Therefore, factors that modulate the activity of NF-κB could potentially regulate inflammatory processes in ischemic stroke. Here, we review the relationship between NF-κB and ischemic stroke, its role in the neurovascular unit, and discuss some animal models that suggest that this relationship is causal.
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影响因子：
8.3
作者：
Nijboer, Cora H. A.;Heijnen, Cobi J.;Kavelaars, Annemieke
通讯作者：
Kavelaars, Annemieke
DOI：
10.1016/s0169-328x(98)00045-x
发表时间：
1998-05-01
期刊：
MOLECULAR BRAIN RESEARCH
影响因子：
--
作者：
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通讯作者：
Cheng, C
影响因子：
2.5
作者：
Irving, EA;Hadingham, SJ;Parsons, AA
通讯作者：
Parsons, AA
影响因子：
5.3
作者：
Cho, S;Park, EM;Iadecola, C
通讯作者：
Iadecola, C
影响因子：
64.8
作者：
BEG, AA;SHA, WC;BALTIMORE, D
通讯作者：
BALTIMORE, D