Stroke: molecular mechanisms and potential targets for treatment.
Stroke: molecular mechanisms and potential targets for treatment.
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DOI：
10.2174/1566524033479717
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发表时间：
2003-05
影响因子：
2.5
通讯作者：
Z. Zheng;J. E. Lee;M. Yenari
中科院分区：
文献类型：
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作者：
Z. Zheng;J. E. Lee;M. Yenari
在过去的几年里，关于缺血性细胞死亡的细胞和分子事件已经取得了重大进展。由于代谢储备的损失、细胞内钙的过度积累、氧化应激和炎症反应的增强，大脑会遭受缺血性损伤。神经元也可能通过坏死或凋亡机制死亡，具体取决于损伤的性质和严重程度。尽管人们普遍认为缺血会导致蛋白质合成停止，但血液供应略有减少的大脑区域尤其能够表达多种基因，其中许多基因的功能才刚刚开始被了解。再灌注和再氧合时基因表达也会上调。因此，许多信号传导途径已被识别，并且现在已知它们有助于缺血进展，或者在某些情况下，有助于自我保护。本综述将重点关注应激基因、凋亡相关基因和炎症的作用。对此类分子事件的了解激发了人们对开发特定分子靶标的兴趣，希望有一天能够影响临床中风的结果。
Significant advances have been made over the past few years concerning the cellular and molecular events underlying ischemic cell death. The brain succumbs to ischemic injury as a result of loss of metabolic stores, excessive intracellular calcium accumulation, oxidative stress, and potentiation of the inflammatory response. Neurons can also die via necrotic or apoptotic mechanisms, depending on the nature and severity of the insult. While it has been widely held that ischemia is notable for cessation of protein synthesis, brain regions with marginal reduction in blood supply are especially capable of expressing a variety of genes, the functions of many of which are only beginning to be understood. Gene expression is also upregulated upon reperfusion and reoxygenation. As a result, a number of signaling pathways have been identified and are now known to contribute to ischemic progression or, in some cases, attempts at self preservation. This review will focus on the roles of stress genes, apoptosis-related genes, and inflammation. Knowledge of such molecular events has fueled interest in developing specific molecular targets with the hope of someday affecting outcome in clinical stroke.