Abstract: Ischemic stroke is a serious medical event that cannot be predicted in advance and can have longlasting effects on patients, families, and communities. A deeper understanding of the changes in gene expression and the fundamental molecular mechanisms involved could help address this critical issue. In recent years, research into regulatory long non-coding (lnc)RNAs, a diverse group of RNA molecules with regulatory functions, has emerged as a promising direction in the study of cerebral infarction. This review paper aims to provide a comprehensive exploration of the roles of regulatory lncRNAs in cerebral infarction, as well as potential strategies for their application in clinical settings. LncRNAs have the potential to act as “sponges” that attract specific microRNAs, thereby regulating the expression of microRNA target genes. These interactions influence various aspects of ischemic stroke, including reperfusion-induced damage, cell death, immune responses, autophagy, angiogenesis, and the generation of reactive oxygen species. We highlight several regulatory lncRNAs that have been utilized in animal model treatments, including lncRNA NKILA, lncRNA Meg8, and lncRNA H19. Additionally, we discuss lncRNAs that have been used as biomarkers for the diagnosis and prognosis of cerebral infarction, such as lncRNA FOXO3, lncRNA XIST, and lncRNA RMST. The lncRNAs hold potential for genetic-level treatments in patients. However, numerous challenges, including inefficiency, low targeting accuracy, and side effects observed in preliminary studies, indicate the need for thorough investigation. The application of lncRNAs in ischemic stroke presents challenges that require careful and extensive validation.

Key words: adeno-associated virus, angiogenesis, autophagy, gene therapy, ischemic stroke, long non-coding RNAs, neuroinflammation, oxidative stress, pathophysiological mechanism, stroke