Dysregulation of serum hsa_circ_0005870 serves as a biomarker to predict disease onset and short-term prognosis in acute coronary syndrome patients

Acute coronary syndrome (ACS) is a leading cause of cardiovascular mortality, but early biomarkers for disease prediction remain limited. Circular RNAs (circRNAs) have emerged as potential diagnostic tools due to their stability and disease-specific expression. The aim of this study is to explore the hsa_circ_0005870 as a diagnostic/prognostic biomarker for ACS and its mechanism. This study enrolled 98 ACS, 68 stable coronary artery disease (SCHD), and 56 controls. Serum hsa_circ_0005870 and miR-127-3p levels were quantified via RT-qPCR. The diagnostic utility of hsa_circ_0005870 was evaluated by receiver operating characteristic (ROC) analysis. Kaplan-Meier survival analysis and multivariate Cox regression assessed independent prognostic factors. CCK-8/flow cytometry measured cell viability/apoptosis; ELISA quantified endothelial dysfunction (ED) markers. Dual-luciferase assays confirmed hsa_circ_0005870-miR-127-3p and miR-127-3p-CDH1 interactions. Serum hsa_circ_0005870 levels were significantly reduced in SCHD and ACS compared to controls. The expression level inversely correlated with Gensini scores. ROC analysis revealed high diagnostic accuracy of hsa_circ_0005870 for distinguishing ACS from both healthy and SCHD. Low expression level elevates the risk of major adverse cardiovascular events. Overexpression of hsa_circ_0005870 promotes cell proliferation, inhibits apoptosis, and suppresses endothelial adhesion molecules. miR-127-3p had opposite effects, negatively correlating with hsa_circ_0005870. Mechanistically, hsa_circ_0005870 negatively regulates miR-127-3p, while miR-127-3p directly targets CDH1. These findings suggest that hsa_circ_0005870 may serve as a potential diagnostic/prognostic biomarker for ACS, modulating cellular viability and apoptosis through miR-127-3p/CDH1 axis-mediated mechanisms while synergistically influencing ACS progression with molecular mediators.