ORIGINAL RESEARCH article
Front. Cardiovasc. Med.
Sec. General Cardiovascular Medicine
Clinical significance analysis of LncRNA HOXA11-AS in regulating vascular endothelial cell function in acute myocardial infarction
Hailong Zhang 1
Xiaolong Wang 1
Jun Du 1
Jialin Qi 2
Xiaoli Qi 1
1. Shengli Oilfield Central Hospital, Dongying, China
2. Shandong Second Medical University, Weifang, China
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Abstract
Objective: Acute myocardial infarction (AMI), a major global health threat, desperately needs new biomarkers. Long non-coding RNA Homeobox A11 HOXA11 antisense RNA (HOXA11-AS), a key cardiovascular regulator, has unclear clinical value in AMI and endothelial dysfunction. This study focuses on these issues. Methods: 118 patients and 100 controls were enrolled. Serum HOXA11-AS levels were quantified via real-time quantitative reverse transcription PCR, and diagnostic value was evaluated using receiver operating characteristic curves. Kaplan-Meier curves evaluate major adverse cardiovascular events (MACEs); Cox regression identified MACE-related factors. Human coronary artery endothelial cells underwent hypoxia/reoxygenation (H/R). Cell viability was detected by Cell Counting kit-8. Levels of superoxide dismutase (SOD), lactate dehydrogenase (LDH), inflammatory factors, and vascular endothelial growth factors (VEGF) were determined via commercial kits and Enzyme-linked immunosorbent assay. Dual-luciferase report and RNA immunoprecipitation assays verified gene-targeting. Results: AMI patients exhibit increased serum HOXA11-AS and decreased miR-24-3p. HOXA11-AS shows a positive link with myocardial injury markers (troponin I, creatine kinase isoenzyme) in AMI. It has 82.20% sensitivity and 78.00% specificity for AMI diagnosis. Elevated HOXA11-AS raises the risk of MACEs, acting as a risk factor. H/R upregulates endothelial HOXA11-AS and downregulates miR-24-3p. H/R reduces cell viability, boosts LDH, inflammatory factors, VEGF, and endothelin-1, while curbing SOD and endothelial nitric oxide synthase (eNOS), inducing endothelial dysfunction. Downregulating HOXA11-AS reverses these, and reducing miR-24-3p partially offsets this reversal. Conclusion: HOXA11-AS serves as a diagnostic biomarker for AMI and indicates a poor prognosis regarding MACEs. Silencing HOXA11-AS mitigates endothelial damage in AMI via miR-24-3p, offering potential new strategies for AMI management.
Summary
Keywords
AMI, Endothelial damage, HOXA11-AS, MACE, miR-24-3p
Received
20 November 2025
Accepted
29 January 2026
Copyright
© 2026 Zhang, Wang, Du, Qi and Qi. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Hailong Zhang
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