ArticleJournal of biochemical and molecular toxicology2022
MicroRNA-454 modulates the oxidative stress and neuronal apoptosis after cerebral ischemia/reperfusion injury via targeting NADPH oxidase 4 (NOX4).
Article in Journal of biochemical and molecular toxicology, 2022. 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, 10 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
- Therapeutic Effects of Zhilong Huoxue Tongyu Capsule on Oxidative Stress and Neuroprotection in a Rat Model of Intracerebral Hemorrhage.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026Article
- Integrated analysis of porcine brain microRNA profiles following pediatric diffuse traumatic brain injury.Acta neuropathologica communications · 2026Article
- Human Neural Progenitor Cell-Derived Exosomes Deliver miR- 100 - 5p Targeting NOX4 mRNA to Alleviate Oxidative Stress in Acute Ischemia Injury.Molecular neurobiology · 2025Article
- MicroRNAs in the Regulation of NADPH Oxidases in Vascular Diabetic and Ischemic Pathologies: A Case for Alternate Inhibitory Strategies?Antioxidants (Basel, Switzerland) · 2022Review
- MicroRNA-454 modulates the oxidative stress and neuronal apoptosis after cerebral ischemia/reperfusion injury via targeting NADPH oxidase 4 (NOX4).Journal of biochemical and molecular toxicology · 2022Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To investigate the function of miR-454 in ischemic stroke, this study was carried out. Cerebral ischemia/reperfusion (I/R) injury animal model and a SHSY5Y cell culture model of oxygen-glucose deprivation/reoxygenation (OGD/R) were constructed. The effects of miR-454 were detected by evaluating the levels of biochemical markers, gene expression, and pathophysiological markers. The results showed that NOX4 level was elevated, while miR-454 expression was reduced in I/R brain samples and in OGD/R-treated cells. The miR-454 agomir declined NOX4 level and reactive oxygen species (ROS) production in rats suffering from I/R. Furthermore, microRNA-145 (miR-454) overexpression inhibited NOX4 level and ROS production in cells treated by OGD/R and decreased luciferase activity in cells transfected with NOX4-wild type (WT) reporter plasmid. Meanwhile, our results proved that the protected effects of miR-454 on SH-SY5Y cells treated by OGD/R were reversed by pcDNA-NOX4 transfection. MiR-454 protected animals from brain injury induced by cerebral I/R via directly regulating its target gene NOX4, illustrating a curatively potential target for treating ischemic stroke.
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