OBJECTIVE: Coronary heart disease (CHD) is a common cardiovascular disease with high incidence and mortality rates. This study aims to explore the role of KMT2E-AS1 in the progression of CHD and its potential regulatory mechanisms. METHODS: The research included 135 CHD patients and 103 healthy volunteers. And CHD patients were categorized into major adverse cardiovascular events (MACE) and non-MACE groups. Differential expression of KMT2E-AS1 in various groups and its diagnostic value were analyzed. Correlation of KMT2E-AS1 expression with myocardial injury markers was investigated. The predictive potential of KMT2E-AS1 for MACE risk was evaluated. The interaction between KMT2E-AS1 and miR-2681-5p was verified, and their effects on human aortic smooth muscle cells (HASMCs) proliferation, inflammation, and oxidative stress response were examined. RESULTS: KMT2E-AS1 is significantly downregulated in the CHD and MACE group. KMT2E-AS1 is significantly negatively correlated with myocardial injury markers, such as Gensini score, creatine kinase-myocardial band, cardiac troponin I, and N-terminal pro-B-type natriuretic peptide. KMT2E-AS1 exhibits favorable diagnostic performance for the occurrence of CHD and serves as an independent protective factor against MACE following surgery. KMT2E-AS1 directly targets and regulates miR-2681-5p. Moreover, KMT2E-AS1 overexpression promotes proliferation, alleviates inflammation, and oxidative stress response in oxidized low-density lipoprotein-induced HASMCs, while miR-2681-5p overexpression counteracts the effects of KMT2E-AS1 overexpression. CONCLUSION: KMT2E-AS1 is a promising biomarker for predicting CHD occurrence and postoperative MACE risk. KMT2E-AS1 protects HASMCs and inhibits CHD progression by targeting miR-2681-5p.
Zhang et al. (Tue,) studied this question.
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