Abstract

Background Non-invasive screening of acute coronary syndromes (ACS) is a clinical challenge. Considering the significance of microRNAs (miRNAs), the significance of miR-629–5p in the onset and development of ACS was assessed, aiming to explore a novel biomarker. Methods This study compared serum miR-629–5p between 115 ACS patients and 103 chest pain cases. The significance of serum miR-629–5p in screening ACS onset, predicting risk, development, and outcomes was evaluated. Additionally, to reveal the regulatory mechanism underlying miR-629–5p, in vitro cellular evaluation was conducted with hypoxia/reoxygenation (H/R)-induced H9c2 cells. The effect of miR-629–5p on cell viability, inflammation, and oxidative stress was investigated. Results Decreasing serum miR-629–5p levels in ACS patients could predict the risk of disease onset, significantly discriminated ACS patients, and predicted adverse outcomes of ACS patients. miR-629–5p showed significant negative correlations with creatine kinase-MB (CK-MB) levels D-dimer (D-D), and Fibrinogen (Fig) levels in ACS patients. Significant negative correlation was also observed in the SYNTAX score and Gensini score. In H/R-induced myocardial cells, overexpressing miR-629–5p could alleviate cell injury, improving cell viability, attenuating inflammation, and oxidative stress. MMP16 was predicted as the downstream target of miR-629–5p, which showed contrast dysregulation in H/R-induced H9c2 cells and was negatively regulated by miR-629–5p. The overexpression of MMP16 could reverse the protective effect of miR-629–5p on H/R-induced myocardial cell injury. Conclusion miR-629–5p could be considered as a diagnostic and prognostic biomarker for ACS. miR-629–5p regulates myocardial cell injury by directly targeting MMP16, of great potential in serving as a therapeutic target for ACS.