ArticleNeuropsychiatric disease and treatment2021
MicroRNA-9-3p Aggravates Cerebral Ischemia/Reperfusion Injury by Targeting Fibroblast Growth Factor 19 (FGF19) to Inactivate GSK-3β/Nrf2/ARE Signaling.
Article in Neuropsychiatric disease and treatment, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.
- Modulation of miRNAs by Phytochemicals in Cerebral Ischemia: A Systematic Review of In Vitro and In Vivo Studies.Phytotherapy research : PTR · 2025Pooled it
- Bile acids in Alzheimer's disease: a double-edged sword in gut-liver-brain signaling and neurodegeneration.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- MicroRNA-9-5p Alleviates Oxidative Stress, Inflammation, and Apoptosis in Cerebral Ischemia-reperfusion Injury by Targeting NOX4Current molecular medicine · 2026Article
- Mendelian Randomization Unlocks Stroke Therapeutics: Dioscin Inhibits CD27-Driven Neuroinflammation via Gut Microbiota Modulation.Molecular neurobiology · 2025Article
- Overexpression of MiR-188-5p Downregulates IL6ST/STAT3/ NLRP3 Pathway to Ameliorate Neuron Injury in Oxygen-glucose Deprivation/Reoxygenation.Current neurovascular research · 2024Article
- Linking Nonalcoholic Fatty Liver Disease and Brain Disease: Focusing on Bile Acid Signaling.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeMicroRNAs (miRNAs) are emerging as essential regulators in the development of cerebral ischemia/reperfusion (I/R) injury. This study aimed to explore the regulation of miR-9-3p on FGF19-GSK-3β/Nrf2/ARE signaling in cerebral I/R injury. MATERIALS AND
methodsA mouse model with I/R injury was constructed by middle cerebral artery occlusion (MCAO) and an HT22 cell model was established by oxygen-glucose deprivation/reperfusion (OGD/R). The expression of miR-9-3p was detected by RT-qPCR. Protein expression of fibroblast growth factor 19 (FGF19), cleaved caspase-3, and GSK-3β signaling-related proteins (p-GSK-3β and Nrf2) were detected by Western blot. Cell viability was assessed by MTT assay. Oxidative stress was detected by commercial kits. The target of miR-9-3p was predicted by TargetScan and confirmed by luciferase reporter assay. The effects of miR-9-3p on GSK-3β/Nrf2/ARE signaling were assessed by rescue experiments.
resultsMiR-9-3p was significantly upregulated in brain tissues of MCAO/R-treated mice and OGD/R-treated HT22 cells. Downregulation of miR-9-3p attenuated infarct volume and neurological outcomes of MCAO/R-treated mice in vivo and OGD/R-induced cell injury and oxidative stress in vitro, while overexpression of miR-9-3p showed the opposite effects. MiR-9-3p directly bound to the 3'-untranslated region of FGF19 and negatively regulated its expression. Inhibition of miR-9-3p enhanced GSK-3β/Nrf2/ARE signaling-mediated antioxidant response, while this effect was partially eliminated by FGF19 or Nrf2 silencing.
conclusionOur study suggests that inhibition of miR-9-3p protects against cerebral I/R injury through activating GSK-3β/Nrf2/ARE signaling-mediated antioxidant responses by targeting FGF19, providing a potential therapeutic target for ischemic stroke.
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