期刊
FEBS JOURNAL
卷 274, 期 13, 页码 3210-3217出版社
WILEY
DOI: 10.1111/j.1742-4658.2007.05890.x
关键词
Bcl-2; brain protection; cerebral ischemia; CREB; glutamate; hypoxia; ischemic tolerance; neurogenesis; neuron; phosphodiesterase inhibitor
Cerebral ischemia triggers robust phosphorylation of cAMP response element-binding protein (CREB) and CRE-mediated gene expression in neurons. Glutamate receptor activation and subsequent calcium influx may activate CREB shortly after ischemia. CREB activation leads to expression of genes encoding neuroprotective molecules, such as the antiapoptotic protein Bcl-2, and contributes to survival of neurons after ischemic insult. Recent studies have suggested that CREB may be involved in acquisition of ischemic tolerance, a phenomenon that occurs after sublethal ischemic stress. CREB activation is also involved in the survival of newborn neurons in the dentate gyrus of the hippocampus after ischemia. Therefore, CREB-related therapeutics may be promising for brain protection and endogenous neurogenesis and could promote functional recovery in ischemic stroke patients. This minireview summarizes our current understanding for the role of CREB in regulating CRE-mediated gene expression during cerebral ischemia.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据