Epigenetic mechanisms and potential therapeutic targets in stroke

被引:20
作者
Morris-Blanco, Kahlilia C. [1 ]
Chokkalla, Anil K. [1 ]
Arruri, Vijay [1 ]
Jeong, Soomin [1 ,2 ]
Probelsky, Samantha M. [1 ]
Vemuganti, Raghu [1 ,2 ,3 ]
机构
[1] Univ Wisconsin, Dept Neurol Surg, Mail Code CSC 8660,600 Highland Ave, Madison, WI 53792 USA
[2] Univ Wisconsin, Neurosci Training Program, Madison, WI 53792 USA
[3] William S Middleton Mem Vet Adm Med Ctr, Madison, WI USA
基金
美国国家卫生研究院;
关键词
Biomarkers; cerebral ischemia; epigenomics; hemorrhagic stroke; neuroprotection; LONG NONCODING RNA; HISTONE DEACETYLASE INHIBITION; ISCHEMIA-REPERFUSION INJURY; COMPETING ENDOGENOUS RNA; FOCAL CEREBRAL-ISCHEMIA; DNA METHYLATION; VALPROIC ACID; NEURONAL DEATH; RAT MODEL; PROMOTER METHYLATION;
D O I
10.1177/0271678X221116192
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Accumulating evidence indicates a central role for epigenetic modifications in the progression of stroke pathology. These epigenetic mechanisms are involved in complex and dynamic processes that modulate post-stroke gene expression, cellular injury response, motor function, and cognitive ability. Despite decades of research, stroke continues to be classified as a leading cause of death and disability worldwide with limited clinical interventions. Thus, technological advances in the field of epigenetics may provide innovative targets to develop new stroke therapies. This review presents the evidence on the impact of epigenomic readers, writers, and erasers in both ischemic and hemorrhagic stroke pathophysiology. We specifically explore the role of DNA methylation, DNA hydroxymethylation, histone modifications, and epigenomic regulation by long non-coding RNAs in modulating gene expression and functional outcome after stroke. Furthermore, we highlight promising pharmacological approaches and biomarkers in relation to epigenetics for translational therapeutic applications.
引用
收藏
页码:2000 / 2016
页数:17
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