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<p>Coronary artery disease (CAD) is a common cardiovascular disorder strongly associated with glutamine metabolism. This study seeks to identify novel glutamine metabolism-related gene markers in CAD.&#xa0;Based on GEO datasets and glutamine metabolism-related genes, hub genes were pinpointed through WGCNA combined with LASSO, SVM-RFE, and random forest algorithms. Immune cell infiltration was estimated with the CIBERSORT algorithm. To confirm the expression and roles of hub genes, ox-LDL-stimulated HUVECs were analyzed in culture.&#xa0;MYBPC3 and TRIM47 emerged as candidate diagnostic signatures for CAD. Associations between MYBPC3/TRIM47 and immune cell infiltration were revealed. Upregulation of MYBPC3 and TRIM47 in CAD was confirmed in both GSE113079 and ox-LDL-treated HUVECs. Knockdown of TRIM47 or MYBPC3 promoted ox-LDL-induced proliferation of HUVECs, alleviated cellular apoptosis, and suppressed the expression of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) as well as M1 macrophage polarization.&#xa0;MYBPC3 and TRIM47 may serve as candidate diagnostic signatures for CAD.</p>

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Application of glutamine metabolism-related gene signatures in the non-invasive diagnosis of coronary artery disease: integrating bulk and single-cell transcriptomics

  • 期刊论文

  • 发表日期：

    2026年7月30日

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  • Zhiyong Zhao,
  • Yu Li,
  • Junpeng Li,
  • Yongqian Gao,
  • Zhijun Yan,
  • Hui Li,
  • Qiuli Liu

摘要

Coronary artery disease (CAD) is a common cardiovascular disorder strongly associated with glutamine metabolism. This study seeks to identify novel glutamine metabolism-related gene markers in CAD. Based on GEO datasets and glutamine metabolism-related genes, hub genes were pinpointed through WGCNA combined with LASSO, SVM-RFE, and random forest algorithms. Immune cell infiltration was estimated with the CIBERSORT algorithm. To confirm the expression and roles of hub genes, ox-LDL-stimulated HUVECs were analyzed in culture. MYBPC3 and TRIM47 emerged as candidate diagnostic signatures for CAD. Associations between MYBPC3/TRIM47 and immune cell infiltration were revealed. Upregulation of MYBPC3 and TRIM47 in CAD was confirmed in both GSE113079 and ox-LDL-treated HUVECs. Knockdown of TRIM47 or MYBPC3 promoted ox-LDL-induced proliferation of HUVECs, alleviated cellular apoptosis, and suppressed the expression of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) as well as M1 macrophage polarization. MYBPC3 and TRIM47 may serve as candidate diagnostic signatures for CAD.