ArticleNeuropsychiatric disease and treatment2025
Integrated Bioinformatics Identifies NLRP3 Inflammasome Hub Genes and Therapeutic Targets in Schizophrenia.
Article in Neuropsychiatric disease and treatment, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- The NLRP3 inflammasome: pathophysiology and therapeutic implications for schizophrenia and neuropsychiatric disorders.Molecular psychiatry · 2026Review
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Authors and funding
8 authors.
Funding
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Abstract
Background: The pathogenesis of schizophrenia (SZ) remains incompletely understood; although neuroinflammation and the NLRP3 inflammasome have been implicated, the key regulatory genes involved are still unidentified. Objective: To investigate the association between SZ and NLRP3 inflammasome-related genes, and to screen for hub genes as potential biomarkers and therapeutic targets. Methods: We analyzed the GEO dataset GSE27383, comprising 43 SZ patients and 29 controls, and identified 1,672 differentially expressed genes (DEGs). NLRP3-related genes were obtained from GeneCards, and weighted gene co-expression network analysis (WGCNA) highlighted the green, yellow, and red modules. The intersection of DEGs, NLRP3-related genes, and module genes was further refined using LASSO and Random Forest algorithms. Immune cell infiltration was profiled with CIBERSORT, and the diagnostic utility of candidate genes was evaluated using ROC curves. Molecular docking was performed to predict compound binding, and hub gene expression was validated in an independent cohort of 20 SZ patients and 20 controls using RT-qPCR on PBMCs. Results: Five hub genes-HSPA8, SCAP, FLNA, TRAF2, and PINK1-AS-were significantly down-regulated in SZ (P < 0.05). The combined ROC-AUC reached 0.883. Molecular docking revealed strong binding affinities of ellagic acid to FLNA (-4.70 kcal mol Conclusion: Five genes (HSPA8, SCAP, FLNA, TRAF2, PINK1-AS) were identified as potential novel biomarkers and therapeutic targets for SZ, providing a theoretical foundation for elucidating disease mechanisms and advancing precision medicine in SZ.
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