Regulation of gene expression in ischemic preconditioning in the brain.
Regulation of gene expression in ischemic preconditioning in the brain.
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发表时间：
2017-12
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通讯作者：
Tuo Yang;Qianqian Li;Feng Zhang
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作者：
Tuo Yang;Qianqian Li;Feng Zhang
中风是第三大死亡原因和长期残疾的主要原因，有效的治疗方法很少，在寻找新的治疗方法方面进展有限。亚致死性缺血损伤诱导对随后严重缺血的保护的现象，称为缺血预处理（IPC），代表了对缺血性脑损伤的内源性保护方法，并可能指导未来治疗策略的突破。人们普遍认为，IPC介导的长期神经保护作用需要新的蛋白质合成;然而，对其相关的调控机制知之甚少。在本综述中，我们总结了基于基因组学的研究，改变基因表达和蛋白质合成，特别是分类潜在的IPC调节途径。我们还回顾了表观遗传学的作用，一个遗传的遗传调控机制，没有改变DNA序列，在IPC介导的神经保护。
Stroke is the third leading cause of death and the leading cause of long-term disability, with very few effective treatments and limited progress in the effort to search for novel therapeutic approaches. The phenomenon that a sublethal ischemic insult induces protection against a subsequent severe ischemia, termed ischemic preconditioning (IPC), represents an endogenous protective approach against ischemic brain injury, and may direct a breakthrough to future therapeutic strategies. It is broadly accepted that new protein synthesis is required for IPC-mediated long-term neuroprotection; however, their relative regulatory mechanisms are poorly understood. In the present review, we summarize genomic-based studies on alterations in gene expression and protein synthesis, particularly categorizing potential pathways regulated by IPC. We also review the role of epigenetics, an inheritable genetic regulatory mechanism without changes in DNA sequence, in IPC-mediated neuroprotection.