ArticleMolecular neurobiology2025
Identification, Clinical Values, and Prospective Pathway Signaling of Lipid Metabolism Genes in Epilepsy and AED Treatment.
Article in Molecular neurobiology, 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.
- Exploring the causal impact of mitochondrial dysfunction on epilepsy: a mendelian randomization study.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas · 2026Article
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Authors and funding
6 authors.
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Abstract
The dysregulation of lipid metabolism has been associated with the etiology and progression of the neurological pathology. However, the roles of lipid metabolism and the molecular mechanism in epilepsy and the use of antiepileptic drugs (AEDs) are relatively understudied. Gene expression profiles of GSE143272 from blood samples were included for differential analysis, and the lipid metabolism-related differentially expressed genes (DEGs) were identified. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed. The STRING database and Cytoscape software were used to establish and visualize protein-protein interaction (PPI) networks. RT-PCR and western blotting were used to verify the expression levels of lipid metabolism-related DEGs in serum and cerebrospinal fluid (CSF). Eleven lipid metabolism-related DEGs were identified including CXCL8, PTGS2, FOSB, G0S2, HLA-C, CLEC12A, ARG1, ELANE, RSAD2, CTSG, and DEFA1. And among them, five lipid metabolism-related Hub DEGs including CXCL8, PTGS2, ELANE, CTSG, and ARG1 were finally verified in serum samples of epilepsy patients. Moreover, CXCL8 was selected and validated in the epilepsy without AEDs and epilepsy with AEDs. G0S2 was significantly decreased in serum and CSF in epilepsy with AEDs compared to epilepsy without AEDs. Collectively, these findings suggest that lipid metabolism is closely related to epilepsy. This revelation opens up opportunities to further investigate the associated molecular mechanisms and possible therapeutic targets for epilepsy.
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