Epigenetic mechanisms of neuroplasticity and the implications for stroke recovery

被引:78
|
作者
Felling, Ryan J. [1 ]
Song, Hongjun [2 ,3 ]
机构
[1] Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21287 USA
[2] Johns Hopkins Univ, Sch Med, Inst Cell Engn, Baltimore, MD 21205 USA
[3] Johns Hopkins Univ, Sch Med, Solomon Snyder Dept Neurosci, Baltimore, MD 21205 USA
基金
美国国家卫生研究院;
关键词
DNA methylation; Histone; MiRNA; Ischemia; Neurogenesis; Axon growth; Synaptogenesis; MESSENGER-RNA EXPRESSION; FOCAL CEREBRAL-ISCHEMIA; CELL SELF-RENEWAL; DNA METHYLATION; EMERGING ROLE; MICRORNA-124; PROTECTS; NEURONAL DEVELOPMENT; ADULT NEUROGENESIS; GENE-EXPRESSION; STEM-CELLS;
D O I
10.1016/j.expneurol.2014.09.017
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Ischemic stroke is a devastating brain injury and an important cause of neurologic disability worldwide and across the lifespan. Despite the physical, social, and economic burdens of this disease there is only a single approved medicine for the treatment of acute stroke, and its use is unfortunately limited to the small fraction of patients presenting within the narrow therapeutic window. Following stroke, there is a period of plasticity involving cell genesis, axon growth, and synaptic modulation that is essential to spontaneous recovery. Treatments focusing on neuroprotection and enhancing recovery have been the focus of intense preclinical studies, but translation of these treatments into clinical use has been disappointing thus far. The important role of epigenetic mechanisms in disease states is becoming increasingly apparent, including in ischemic stroke. These regulators of gene expression are poised to be critical mediators of recovery following stroke. In this review we discuss evidence for the role of epigenetics in neuroplasticity and the implications for stroke recovery. (C) 2014 Elsevier Inc. All rights reserved.
引用
收藏
页码:37 / 45
页数:9
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