Abstract

Stroke is a major cause of premature mortality and disability around the world. Therefore, identification of cellular and molecular processes implicated in the pathogenesis and progression of ischemic stroke has become a priority. Long non-coding RNAs (lncRNAs) are emerging as significant players in the pathophysiology of cerebral ischemia. They are involved in different signalling pathways of cellular processes like cell apoptosis, autophagy, angiogenesis, inflammation, and cell death, impacting the progression of cerebral damage. Exploring the functions of these lncRNAs and their mechanism of action may help in the development of promising treatment strategies. In this review, the current knowledge of lncRNAs in ischemic stroke, focusing on the mechanism by which they cause cellular apoptosis, inflammation, and microglial activation, has been summarized. Very few lncRNAs have been functionally annotated. Therefore, the therapies based on lncRNAs still face many hurdles since the potential targets are likely to increase with the identification of new ones. Majority of experiments involving the identification and function of lncRNAs have been carried out in animal models, and the role of lncRNAs in human stroke presents a challenge. However, mitigating these issues through more rational experimental design might lead to the development of lncRNA-based stroke therapies to treat ischemic stroke.

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