Abstract

Ischemic stroke (IS) is an acute cerebral vascular event with high mortality and morbidity. Though the precise pathophysiologic routes leading to this condition are not entirely clarified, growing evidence from animal and human experiments has exhibited the impact of non-coding RNAs in the pathogenesis of IS. Various lncRNAs namely MALAT1, linc-SLC22A2, linc-OBP2B-1, linc_luo_1172, linc-DHFRL1-4, SNHG15, linc-FAM98A-3, H19, MEG3, ANRIL, MIAT, and GAS5 are possibly involved in the pathogenesis of IS. Meanwhile, lots of miRNAs contribute in this process. Differential expression of lncRNAs and miRNAs in the sera of IS patients versus unaffected individuals has endowed these transcripts the aptitude to distinguish at risk patients. Despite conduction of comprehensive assays for evaluation of the influence of lncRNAs/miRNAs in the pathogenesis of IS, therapeutic impacts of these transcripts in IS have not been clarified. In the present paper, we review the impact of lncRNAs/miRNAs in the pathobiology of IS through assessment of evidence provided by human and animal studies.

Highlights

  • Ischemic stroke (IS) is an acute cerebrovascular event with high mortality and morbidity

  • Assessment of long non-coding RNAs (lncRNAs) signature at two time points after IS has revealed differential expression of 3,009 and 2,034 lncRNAs 24 h and 7 days after IS, respectively. These results have shown the impact of IS on lncRNA signature at both the acute and subacute phases

  • H19 precludes the development of neurogenesis after IS via p53/Notch1 pathway (Wang et al, 2019a)

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Summary

INTRODUCTION

Ischemic stroke (IS) is an acute cerebrovascular event with high mortality and morbidity. NcRNAs and Stroke miRNAs comprise an ever-growing type of non-coding RNAs that target specific sequences in the 3 untranslated regions of genes, decreasing their expression via mRNA degradation or translation blocking (O’Brien et al, 2018). These transcripts are about 22 nucleotides in length. H19 precludes the development of neurogenesis after IS via p53/Notch pathway (Wang et al, 2019a) Another experiment has reported association between H19 and Acute Stroke Treatment (TOAST) subclasses of atherosclerotic patients.

27 IS patients
10 AIS patients and 10 healthy controls 96 AIS patients
H19 MALAT1
60 ICR mice 16 SD rats SD rats
DISCUSSION
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