Background <p>Endothelial dysfunction is the initiating factor in atherosclerosis and is a persistent feature throughout the entire course of acute myocardial infarction (AMI). Circular RNA (circRNA) fulfils a vital regulatory role in cardiovascular diseases, including AMI.</p> Aim <p>To investigate the expression and clinical significance of circ_0089762 in AMI, and to elucidate the molecular mechanism in regulating hypoxia/reoxygenation (H/R)-induced damage in human umbilical vein endothelial cells (HUVECs).</p> Methods <p>Serum levels of circ_0089762, miR-938, and STAT3 were measured by RT-qPCR. A model H/R injury model was established in HUVECs, and by transfecting to modulate circ_0089762, miR-938, assess cell viability, apoptosis, migration, oxidative stress, and inflammation levels. The targeting relationship was validated using dual-luciferase assays. Rescue experiments were conducted to verify the regulatory axis.</p> Results <p>circ_0089762 is hyper-expressed in AMI, and it has certain diagnostic accuracy in distinguishing AMI patients from healthy individuals, as well as being associated with major adverse cardiovascular events (MACE). H/R treatment can upregulate circ_0089762 expression. Silencing circ_0089762 enhances cell viability, inhibits apoptosis, improves migration, and reduces MDA levels whilst increasing NO and SOD levels, and suppresses the release of inflammatory factors. circ_0089762 directly targets miR-938, and miR-938 directly targets STAT3. Inhibition of miR-938 reverses the protective effects of circ_0089762 knockdown, and further knockdown of STAT3 restores the endothelial protective effects.</p> Conclusion <p>circ_0089762 exacerbates H/R-induced apoptosis, oxidative stress, and inflammatory response in HUVECs by regulating miR-938 and STAT3 expression. circ_0089762 may act as a potential biomarker for the diagnosis, prognostic assessment, and targeted treatment of AMI.</p>