ANALYZING SERUM MOTS-C, MIR-146A, AND RBP4 LEVELS IN ATHLETES: CORRELATIONS WITH CORONARY ARTERY DISEASE SEVERITY AND IMPLICATIONS FOR CARDIOVASCULAR HEALTH MONITORING
Keywords:
Serum Mitochondria-Derived Peptide; MiR-146a; Retinol-Binding Protein 4; coronary heart disease; coronary artery diseaseAbstract
This study examines the serum levels of mitochondria-derived peptide (MOTS-c), miR-146a, and retinol-binding protein 4 (RBP4) in athletes with varying degrees of coronary artery disease (CAD), potentially linked to their intense physical training regimes. We analyzed the data of 90 patients diagnosed with coronary heart disease (CHD), who were admitted to our hospital between August 2020 and March 2022, alongside 30 healthy controls. Participants were categorized based on coronary angiography (CAG) results into three groups: stable angina pectoris (SAP), unstable angina pectoris (UAP), and acute myocardial infarction (AMI), with 30 subjects in each category. Our analysis revealed distinct variations in the expressions of MOTS-c, miR-146a, and RBP4 across the groups, correlating with the severity of coronary lesions as quantified by the Gensini score. Specifically, MOTS-c levels were inversely associated with disease severity, being lowest in the AMI group and highest in controls. Conversely, levels of miR-146a and RBP4 were elevated in CAD patients compared to controls, with the highest readings in the AMI group. These findings indicate a strong correlation between these biomarkers and the degree of CAD, suggesting their utility in monitoring cardiovascular risks in athletes. The results underscore the potential of these biomarkers as significant indicators of cardiovascular health in athletes, providing a non-invasive method to assess the risks associated with high-intensity sports participation. The correlation of MOTS-c, miR-146a, and RBP4 with the Gensini score highlights their clinical relevance in predicting the severity of CHD, thereby enabling better management and preventative strategies in sports medicine.