Serum and Salivary microRNA Biomarkers Reveal Oxidative Stress Dysregulation in Coronary Artery Disease

Introduction and aim Coronary artery disease (CAD) is a major cause of death. Epicardial adipose tissue (ECAT) contributes to CAD via oxidative stress, regulated by non-coding RNAs like miRNAs and lncRNAs. Methods Oxidative stress-related genes were retrieved from GeneCards. Microarray datasets (GSE64554 and GSE64563) identified differentially expressed genes and miRNAs in ECAT. PPI network and clustering revealed 51 key genes. Bottleneck analysis highlighted CD44, RUNX3, and KLRD1. miR-127-3p, regulating these genes, showed downregulation in ECAT, saliva, and plasma samples from 30 CAD patients. Results Out of 407 overlapping oxidative stress genes, 51 were strongly regulated via miRNA–lncRNA networks. CD44, RUNX3, and KLRD1 were key biomarkers. miR-127-3p showed significant downregulation ( P < .05) and the highest lncRNA interaction count. Its consistent decrease in ECAT, saliva, and plasma indicates systemic dysregulation in CAD. Conclusions CD44, RUNX3, and KLRD1 are oxidative stress biomarkers in ECAT, regulated by miR-127-3p. Its consistent downregulation in ECAT, plasma, and saliva supports its role in CAD pathogenesis and systemic relevance. Clinical relevance The consistent downregulation of miR-127-3p in plasma and saliva highlights its potential as a clinically relevant, non-invasive biomarker, supporting early detection and monitoring strategies for CAD through accessible body fluids.