A narrative review of long noncoding RNA: insight into neural ischemia/reperfusion mediated by two pathophysiological processes of injury and repair

长链非编码RNA的叙述性综述:深入了解由损伤和修复两种病理生理过程介导的神经缺血/再灌注损伤

阅读:1

Abstract

BACKGROUND AND OBJECTIVE: A thorough understanding of the role of long noncoding RNAs (lncRNAs) in cerebral ischemia/reperfusion injury (IRI) is conducive to a comprehensive understanding of the molecular regulatory network of IRI. Such an understanding could be of great significance for finding new biomarkers and therapeutic targets of IRI. Such findings could protect important tissues and organs and improve the clinical prognosis of patients. METHODS: We conducted a literature search for published manuscripts on neural ischemia/reperfusion up to October 2021 in the PubMed, Web of Science, Cochrane Library, and EMBASE databases. KEY CONTENT AND FINDINGS: LncRNAs are a group of regulatory sequences that play a role at the transcriptional, posttranscriptional and epigenetic levels. LncRNAs are highly expressed in the central nervous system and play an important regulatory role in the development of the central nervous system and diseases. The mechanism of IRI is complex, and pathological injury processes, such as apoptosis, oxidative stress injury, neuroinflammation, excitatory amino acid toxicity, autophagy and impaired blood-brain barrier function, are mutually intertwined or promoted. These processes can aggravate the secondary injury of brain tissue after ischemia-reperfusion. Moreover, cerebral IRI can induce a large number of changes to the expression of lncRNAs in the brain, suggesting that lncRNAs are related to the complicated pathological process of cerebral IRI. CONCLUSIONS: In this narrative review, the roles of lncRNAs in cerebral IRI, apoptosis, anti-apoptosis, nerve regeneration, and repair after injury are reviewed. Additionally, possible future research directions for lncRNAs in ischemic stroke injury and repair are proposed.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。