Role of transcription factors in mediating post-ischemic cerebral inflammation and brain damage
Role of transcription factors in mediating post-ischemic cerebral inflammation and brain damage
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DOI：
10.1016/j.neuint.2007.04.019
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发表时间：
2007-06-01
影响因子：
4.2
通讯作者：
Vemuganti, Raghu
中科院分区：
文献类型：
--
作者：
Yi, Jae-Hyuk;Park, Seung-Won;Vemuganti, Raghu
炎症是脑缺血后神经元死亡的已知沉淀剂。促进或抑制炎症在脑中的开始和扩散的机制仍在争论中。由于其调节基因表达的能力，在缺血脑中诱导的几种转录因子可以调节缺血后炎症。虽然认为诸如IRF 1、NF-κ B、ATF-2、STAT 3、Egr 1和C/EBP β的转录因子的诱导促进缺血后炎症，但认为诸如HIF-1、CREB、c-fos、PPAR α、PPAR γ和p53的转录因子的激活预防缺血后炎症和神经元损伤。其中，过氧化物酶体增殖物激活受体γ，这是一种配体激活的转录因子，最近显示，以防止炎症基因的表达，在几种动物模型中枢神经系统疾病。本文综述了局灶性脑缺血后，其激动剂诱导的一些分子机制。(C)2007爱思唯尔有限公司保留所有权利。
Inflammation is a known precipitator of neuronal death after cerebral ischemia. The mechanisms that promote or curtail the start and spread of inflammation in brain are still being debated. By virtue of their capability to modulate gene expression, several transcription factors induced in the ischemic brain can modulate the post-ischemic inflammation. While the induction of transcription factors such as IRF1, NF-kappa B, ATF-2, STAT3, Egrl and C/EBP beta is thought to promote post-ischemic inflammation, activation of transcription factors such as HIF-1, CREB, c-fos, PPAR alpha, PPAR gamma and p53 is thought to prevent post-ischemic inflammation and neuronal damage. Of these, PPAR gamma which is a ligand-activated transcription factor was recently shown to prevent inflammatory gene expression in several animal models CNS disorders. This review article discusses some of the molecular mechanisms of PPAR gamma induction by its agonists following focal cerebral ischemia. (C) 2007 Elsevier Ltd. All rights reserved.