Abstract

Background and ObjectiveA 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.MethodsWe 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 FindingsLncRNAs 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.ConclusionsIn 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.

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