CMS is characterized by the convergence of thyroid dysregulation, inflammation, oxidative stress, and increased ApoE gene expression, which highlights a coordinated molecular network underlying CMS and support the integration of molecular and inflammatory biomarkers into cardiometabolic risk assessment.
Abstract
Abstract Objectives This study aimed to examine the association of thyroid-stimulating hormone (TSH), interleukin-6 (IL-6), and 3-nitrotyrosine (3-NT) with ApoE gene expression and to evaluate their diagnostic utility in CMS. Methods This case–control study compared hormonal, inflammatory, oxidative stress, and gene expression markers between CMS cases and healthy controls. Group differences were analyzed using non-parametric tests. Diagnostic performance was evaluated using receiver operating characteristic (ROC) analysis, and relationships among variables were assessed using correlation and multivariable logistic regression models. Results CMS cases showed significantly higher levels of TSH, IL-6, 3-NT, and ApoE gene expression compared with controls. TSH demonstrated modest diagnostic accuracy (AUC=0.740), whereas 3-NT exhibited excellent discriminative performance (AUC=0.963). IL-6 also showed good diagnostic accuracy. ApoE gene expression demonstrated strong diagnostic performance and was positively correlated with TSH, 3-NT, and IL-6, with the strongest association observed for IL-6. Multivariable regression analysis confirmed that elevated TSH, IL-6, and 3-NT were independently associated with CMS status. Conclusions CMS is characterized by the convergence of thyroid dysregulation, inflammation, oxidative stress, and increased ApoE gene expression. These findings highlight a coordinated molecular network underlying CMS and support the integration of molecular and inflammatory biomarkers into cardiometabolic risk assessment. Larger longitudinal studies are required to confirm these observations.
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