Diagnostic Value of miR-1225-5p in Acute Coronary Syndrome and its Mechanism in ox-LDL Induced Human Coronary Artery Endothelial Cells Injury

Background Acute coronary syndrome (ACS), a life-threatening cardiovascular emergency, faces challenges in early diagnosis and risk stratification. MicroRNAs (miRNAs) have emerged as key regulators in cardiovascular diseases. Objectives To investigate the diagnostic/predictive significance of miR-1225-5p in ACS and its mechanism of regulating human coronary artery endothelial cells (HCAECs) injury induced by ox-LDL via targeting FAS. Methods miR-1225-5p levels in serum were determined by RT-qPCR in 99 ACS patients and controls, with correlation analysis to clinical indicators. HCAECs were used to assess viability, apoptosis, and inflammation/oxidative stress (IL-6, TNF-α, MDA, SOD) via CCK-8, flow cytometry, and ELISA. Target binding between FAS and miR-1225-5p was validated by dual-luciferase reporter and RIP assays, with functional validation experiments. Results miR-1225-5p was significantly downregulated in ACS ( P < 0.001), with subtype-specific patterns (UA > NSTEMI > STEMI). ROC analysis showed high diagnostic accuracy (AUC = 0.885 for ACS; 0.790-0.964 for subtypes). miR-1225-5p (HR = 5.409, 95% CI = 1.281–22.837) and Gensini score (HR = 3.524, 95% CI = 1.066–11.646) acted as a predictive factor in ACS, and downregulated miR-1225-5p is linked to MACEs in ACS patients. Overexpression of miR-1225-5p alleviated ox-LDL-induced HCAECs injury (enhanced viability, suppressed apoptosis, reduced inflammation/oxidative stress). FAS acted as a specific target of miR-1225-5p and is negatively associated with miR-1225-5p (r = -0.721). Overexpression of FAS reversed miR-1225-5p-mediated protective effects on HCAECs. Conclusion miR-1225-5p is a potential diagnostic indicator for ACS and alleviates HCAECs injury by targeting FAS.