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Recent cardiovascular research has highlighted the significant potential of KMT2E-AS1 in CHD as a critical diagnostic and prognostic tool. Coronary heart disease (CHD) remains a leading cause of mortality in India and globally, necessitating the identification of precise molecular markers. Consequently, researchers have focused on long non-coding RNAs (lncRNAs) like KMT2E-AS1 to better understand their regulatory roles in heart health. A recent study involving 135 CHD patients and 103 healthy volunteers revealed that KMT2E-AS1 is significantly downregulated in patients with coronary conditions.
Furthermore, the expression levels of KMT2E-AS1 show a strong negative correlation with established myocardial injury markers. These markers include the Gensini score, creatine kinase-myocardial band (CK-MB), cardiac troponin I (cTnI), and N-terminal pro-B-type natriuretic peptide (NT-proBNP). Therefore, lower levels of KMT2E-AS1 often indicate more severe cardiac damage and a higher risk of postoperative complications. The lncRNA serves as an independent protective factor, and its presence helps clinicians predict the likelihood of major adverse cardiovascular events (MACE) following surgery.
The study also elucidated the specific molecular pathway through which KMT2E-AS1 exerts its protective effects. It functions by directly targeting and regulating miR-2681-5p. In laboratory models using human aortic smooth muscle cells (HASMCs), the overexpression of KMT2E-AS1 promoted cell proliferation and successfully alleviated inflammation. Additionally, this overexpression reduced the oxidative stress response typically induced by oxidized low-density lipoprotein (ox-LDL).
However, the introduction of miR-2681-5p counteracted these beneficial effects. This interaction confirms that the KMT2E-AS1/miR-2681-5p axis is a vital regulator of vascular cell stability. By inhibiting CHD progression through this pathway, KMT2E-AS1 offers a promising target for future therapeutic interventions. Clinicians may eventually use these findings to refine risk stratification and personalize treatment plans for patients at high risk of MACE.
KMT2E-AS1 is significantly downregulated in CHD patients. Its expression levels inversely correlate with myocardial injury markers like troponin and NT-proBNP, making it a favorable diagnostic and predictive tool for cardiovascular risk.
This axis regulates human aortic smooth muscle cells. KMT2E-AS1 protects these cells by reducing inflammation and oxidative stress while promoting healthy cell growth, effectively inhibiting the progression of coronary heart disease.
Yes, research indicates that KMT2E-AS1 acts as an independent protective factor against Major Adverse Cardiovascular Events (MACE). Patients with higher expression levels generally face a lower risk of postoperative complications.
Disclaimer: This content is for informational and educational purposes only and does not constitute medical advice. It is not intended to be a substitute for professional medical judgment, diagnosis, or treatment. Always seek the advice of your physician or other qualified healthcare provider with any questions you may have regarding a medical condition. Refer to the latest local and national guidelines for clinical practice.
References
Zhang J et al. The clinical role and regulatory mechanism of KMT2E-AS1 in coronary heart disease. Coron Artery Dis. 2026 May 05. doi: 10.1097/MCA.0000000000001646. PMID: 42083922.
Tai YY et al. Allele-specific control of rodent and human lncRNA KMT2E-AS1 promotes hypoxic endothelial pathology in pulmonary hypertension. Sci Transl Med. 2024 Jan 10. doi: 10.1126/scitranslmed.add2029.
Lemay SE et al. A HIF-2α-dependent KMT2E-AS1/KMT2E axis orchestrates endothelial epigenetic and metabolic dysfunction in pulmonary hypertension. Ann Transl Med. 2024 May 28. doi: 10.21037/atm-24-11.
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