Evidence map›Paper›PMID 42029101›Full record

ArticleEpilepsia open2026

MiR-30a-5p mediates epileptogenesis in epilepsy models by targeting SOX4 to regulate the Wnt/β-catenin pathway.

Zhenlin Yang, Xu Zhang, Jingjing Guo, Yuanxin Wei, Jinzi Li

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Article in Epilepsia open, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Zhenlin YangDepartment of Pediatrics, Yanbian University Hospital, Yanji, China.
Xu ZhangDepartment of Pediatrics, Yanbian University Hospital, Yanji, China.
Jingjing GuoDepartment of Pediatrics, Yanbian University Hospital, Yanji, China.
Yuanxin WeiDepartment of Pediatrics, Yanbian University Hospital, Yanji, China.
Jinzi LiDepartment of Pediatrics, Yanbian University Hospital, Yanji, China.ORCID https://orcid.org/0000-0002-4739-8605

Funding

Jilin Health Science and Technology Capacity Enhancement Program 2023JC022Scientific Research Program of Jilin Provincial Department of Education JJKH20240693KJ
6 · The paper itself

Abstract

objectiveThe pathogenesis of epilepsy is closely associated with neuronal synaptic plasticity. MicroRNAs (miRNAs) can regulate various biological processes by binding to specific sequences on target genes. This study employs bioinformatics, molecular dynamics, and experimental approaches to investigate the mechanism by which MiR-30a-5p treats epilepsy through targeting SOX4 and regulating the Wnt/β-catenin signaling pathway.

methodsPerformed bioinformatics analysis to predict the signaling pathways involved in miRNA-30a-5p-mediated intervention in epilepsy. RT-qPCR was used to detect the expression levels of miR-30a-5p in the hippocampal tissues of epileptic rats and in primary hippocampal neurons subjected to Mg

resultsThe expression level of miR-30a-5p was significantly elevated in the hippocampal region of epileptic rats and in magnesium-depleted hippocampal neuronal cultures. SOX4 was identified as a direct target of miR-30a-5p. Inhibiting miR-30a-5p reduces the expression of synapse-associated proteins (SYP/CaMKII/PSD95), while upregulating SOX4 and downregulating the levels of Wnt3a, β-catenin, and cyclin D1. miR-30a-5p may participate in alterations of neuronal synaptic plasticity by directly targeting and inhibiting SOX4 expression, thereby activating the Wnt/β-catenin signaling pathway. SIGNIFICANCE: This study provides evidence that miR-30a-5p participates in the process of synaptic plasticity impairment in epileptic neurons. The study confirms a direct interaction between miR-30a-5p and SOX4. Furthermore, miR-30a-5p regulates the Wnt/β-catenin signaling pathway by targeting SOX4, thereby influencing neuronal synaptic plasticity impairment. This discovery provides a novel potential therapeutic target for delaying epilepsy progression. PLAIN LANGUAGE SUMMARY: Epilepsy is a common brain disorder that affects millions of people worldwide. This study found that a small molecule called miR-30a-5p increases in the brain during epilepsy and disrupts normal communication between neurons. By blocking this molecule in laboratory experiments, we were able to improve neuron function and reduce damage. These findings suggest that targeting miR-30a-5p could lead to new treatments to slow down the progression of epilepsy.

Indexed as

EpilepsyHippocampusMicroRNAsSOXC Transcription FactorsWnt Signaling PathwayAnimalsbeta CateninDisease Models, AnimalMaleNeuronal PlasticityNeuronsRatsRats, Sprague-Dawleybeta CateninMicroRNAsMIRN30 microRNA, ratSOXC Transcription FactorsepilepsymiR‐30a‐5pSOX4synaptic plasticityWnt/β‐catenin pathway

Identifiers

PMID42029101
PMCPMC13238734

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.