ArticleBMC neuroscience2026
MEF2A-mediated inhibition of ischemic stroke injury via the PI3K/AKT pathway: a comprehensive bioinformatics and in vitro study.
Article in BMC neuroscience, 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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Abstract
backgroundThrombosis or embolism causes blood flow stoppage, resulting in ischemic stroke (IS), the most frequent clinical cerebrovascular disorder. It accounts for more than 80% of all strokes and has a significant disability and mortality rate. Regulating critical targets to stop the ischemia pathophysiological cascade and preserve brain cells is essential for treating IS.
methodsWe included a deCODE analysis encompassing data on cis-acting variations for 4719 blood proteins. The IS summary statistics consist of 11,929 cases and 472,192 controls. We identified blood proteins associated with IS susceptibility using the Mendelian randomization (MR) method. We comprehensively analyzed the GSE58294 dataset, including differential expression gene identification, functional enrichment analysis, weighted gene co-expression network analysis, least absolute shrinkage and selection operator analysis, and transcription factor identification. The expression patterns of key genes were identified using single-cell sequencing data. The oxygen-glucose deprivation/reperfusion (OGD/R) model was established, and myocyte enhancer factor 2 A (MEF2A) was overexpressed in Neuro-2a/PC12 cells using an overexpression vector. We used CCK-8 and western blotting to observe the cell viability, oxidative stress level, and p-PI3K and p-Akt protein expression.
resultsWe discovered 73 blood proteins related to IS, and the sensitivity analysis findings supported the causal associations. The MR results and bioinformatics underwent a thorough examination, revealing MEF2A as a transcription factor involved in the development of IS. Single-cell sequencing results revealed that MEF2A was mostly expressed in microglia and endothelial cells. Additional in vitro experiments showed that overexpression of MEF2A could significantly mitigate OGD/R-induced Neuro-2a/PC12 cell injury and oxidative stress, potentially associated with increased PI3K/Akt protein production.
conclusionThis study, using MR analysis, transcriptomics, and in vitro experiments, identified the transcription factor MEF2A as a potential target for treatment. This gives preclinical evidence for drug development. CLINICAL TRIAL NUMBER: Not applicable.
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