ArticleMolecular medicine reports2021
Long non‑coding RNA XIST promotes cerebral ischemia/reperfusion injury by modulating miR‑27a‑3p/FOXO3 signaling.
Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- A systematic review of the research progress of non-coding RNA in neuroinflammation and immune regulation in cerebral infarction/ischemia-reperfusion injury.Frontiers in immunology · 2022Pooled it
- Therapeutic Delivery of Phloretin by Mixed Emulsifier-Stabilized Nanoemulsion Alleviated Cerebral Ischemia/Reperfusion Injury.Pharmaceutics · 2025Article
- Sphingomyelin regulates the transcriptional machinery in nuclear lipid microdomains.Communications biology · 2025Article
- Silencing LncRNA HCG27 ameliorates cognitive dysfunction after ischemic stroke via miR-27a-3p regulation.Hereditas · 2025Article
- LINC01123 aggravates cerebral ischemia reperfusion injury by targeting miR-654-5p to upregulate METTL7A.Scientific reports · 2025Article
- An Update on Neuroaging on Earth and in Spaceflight.International journal of molecular sciences · 2025Review
- Serum miR-27a Reduction and FOXO3 Elevation in Elderly Patients with Severe Pneumonia Complicated with ARDS: Association with Disease Severity and Prognosis.Journal of inflammation research · 2025Article
- The Mechanisms of Long Non-coding RNA-XIST in Ischemic Stroke: Insights into Functional Roles and Therapeutic Potential.Molecular neurobiology · 2024Review
- Effect of miR-17 onFrontiers in veterinary science · 2024Article
- The forkhead box O3 (FOXO3): a key player in the regulation of ischemia and reperfusion injury.Cellular and molecular life sciences : CMLS · 2023Review
- Mechanism of lncRNA SNHG16 in oxidative stress and inflammation in oxygen-glucose deprivation and reoxygenation-induced SK-N-SH cells.Bioengineered · 2022Article
- The lncRNAs at X Chromosome Inactivation Center: Not Just a Matter of Sex Dosage Compensation.International journal of molecular sciences · 2022Review
- Identification of programmed cell death-related gene signature and associated regulatory axis in cerebral ischemia/reperfusion injury.Frontiers in genetics · 2022Article
- Acupuncture-Moxibustion Combined with Rehabilitation Training Is Conducive to Improving the Curative Effect, Cognitive Function, and Daily Activities of Patients with Cerebral Infarction.Computational and mathematical methods in medicine · 2022Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cerebral ischemia/reperfusion (I/R) injury leads to neuronal damage, which may cause disability and even mortality. Multiple studies have revealed that long non‑coding RNAs (lncRNAs) serve pivotal roles in the pathogenesis of cerebral I/R injury. Therefore, the present study aimed to investigate whether the lncRNA X inactivate‑specific transcript (XIST) protects neuronal cells from cerebral I/R injury. In the present study, reverse transcription‑quantitative PCR demonstrated that XIST expression was upregulated in the brain tissues of an I/R mouse model and in oxygen and glucose deprivation/reperfusion (OGD/R)‑treated Neuro‑2a (N2a) cells. Knockdown of XIST alleviated cerebral injury, as well as reduced N2a cell apoptosis and reactive oxygen species (ROS) production. Additionally, luciferase reporter and RNA immunoprecipitation assays identified that XIST could bind with microRNA (miR)‑27a‑3p. It was found that miR‑27a‑3p expression was downregulated in the brain tissues of an I/R mouse model and in OGD/R‑induced N2a cells. In addition, miR‑27a‑3p overexpression attenuated I/R‑induced cerebral injury, and inhibited the apoptosis and ROS production of N2a cells. miR‑27a‑3p was found to target FOXO3. Silencing of FOXO3 alleviated cerebral injury, as well as inhibited N2a cell apoptosis and ROS production. Collectively, these findings indicated that XIST aggravated cerebral I/R injury by regulating miR‑27a‑3p/FOXO3 signaling, which may provide a novel insight into the treatment of cerebral I/R injury.
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Registered trials
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