ArticleMolecular biology reports2026
Peripheral immune cell expression of IRAK1, TRAF6, MAPK1 and CXCL8 in coronary artery disease.
Article in Molecular biology reports, 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
backgroundChronic inflammation is involved in the pathogenesis of coronary artery disease (CAD). This case-control study investigated whether the systemic inflammatory response reflects the status of CAD by evaluating the expression of four genes in the IL-1R/TLR pathway (IRAK1, TRAF6, MAPK1, and CXCL8) in peripheral blood mononuclear cells (PBMCs). METHODS AND
resultsThe study involved 125 angiographically confirmed CAD patients and 125 healthy controls. The relative expression levels of IRAK1, TRAF6, MAPK1, and CXCL8 in PBMCs were compared between groups using t-tests. ROC curve analysis was performed and multivariable binary logistic regression was carried out using z-scored ΔCt values for IRAK1, TRAF6, MAPK1, and CXCL8. IRAK1, TRAF6, and MAPK1 showed increased expression in CAD, but this was not statistically significant; CXCL8 was significantly increased (fold change 1.94; p < 0.001). In multivariable logistic regression analysis, only CXCL8 showed an independent relationship with CAD (p < 0.001). ROC curve analysis for CXCL8 had an area under the curve of 0.81, suggesting good discrimination between CAD patients and healthy controls. Further protein-protein interaction network analysis also indicated that IRAK1, TRAF6, and MAPK1 form an integrated upstream signalling module, while CXCL8 acts as a downstream inflammatory mediator.
conclusionsCXCL8 is significantly upregulated in CAD and has a high level of diagnostic discrimination, which argues for its potential utility as an inflammatory marker derived from PBMCs. Network analysis identifies IRAK1, TRAF6, and MAPK1 as an integrated signalling core, with CXCL8 as an inflammatory downstream effector, which further supports the biological plausibility of CXCL8 induction in CAD.
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