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Genes
By Jin Xue, Zhaoxiang Zhang, Wuting Wei and 6 others.
Metabolic reprogramming plays a vital role in subarachnoid hemorrhage (SAH). This study aims to identify biomarkers related to metabolic reprogramming in SAH.
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Transcriptome datasets (GSE36791 and GSE73378) were downloaded from the GEO database, and the metabolic reprogramming-related genes were retrieved from the Molecular Signatures Database. Candidate genes were identified by intersecting differentially expressed genes, WGCNA module genes, and metabolic genes. Hub genes were screened via CytoHubba, machine learning, and Mendelian randomization. ROC curves were generated to evaluate the diagnostic performance of the hub genes. Additionally, functional enrichment analysis, circulating immune-cell composition analysis, and drug prediction were performed. A cellular SAH model (U251 cells) and clinical samples were used for RT-qPCR validation.
Three hub genes (IMPDH2, RPL4, and HSPA1A) were identified to develop a nomogram model, which showed good diagnostic value (AUC = 0.850) in the training dataset GSE36791. Functional analyses revealed that hub genes were involved in multiple processes, including ribosome biosynthesis, purine metabolism, and immune regulation. Circulating immune-cell composition analysis showed that neutrophils were significantly enriched in SAH patients. Molecular docking suggested favorable binding affinities of mycophenolate-IMPDH2, ataluren-RPL4, and carbamazepine-HSPA1A. In clinical samples (eight SAH patients and eight controls), IMPDH2 and RPL4 were downregulated, whereas HSPA1A was upregulated. In the cellular SAH model, IMPDH2 and HSPA1A showed expression trends consistent with the clinical samples, whereas RPL4 did not show a statistically significant difference.
These findings suggest that IMPDH2, RPL4, and HSPA1A may serve as potential diagnostic biomarkers for SAH and as candidate genes for further investigation.
Published in Genes. The abstract is shown as published and remains the work of its authors; read the full article at the source.
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