Circulating Circ_0089762 Predicts Adverse Outcomes in Acute Myocardial Infarction Via Regulating miR‑938/STAT3‑Mediated Endothelial Dysfunction.

Authors

Yun Zhao, Pengfei Lu, Xing Lu, Zhiqiang Liu

Published in

Cardiovascular drugs and therapy. Jul 28, 2026. Epub Jul 28, 2026.

Abstract

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.
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).
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.
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.
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.

PMID:
42518073
Bibliographic data and abstract were imported from PubMed on 28 Jul 2026.

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