LncRNA DLEU1 Regulates TNRC6A Expression to Exacerbate Acute Myocardial Infarction by Adsorbing miR‐23a‐3p

Hypoxia-treated H9c2 cells were used to create an in vitro cells injury model. RT-qPCR analysis revealed DLEU1, miR-23a-3p, and TNRC6A expressions in serum of AMI patients and H9c2 cells. The viability and apoptosis of cardiomyocytes were assessed via the CCK-8 assay and flow cytometry. ELISA assays were employed to detect MDA, SOD, LDH, and CK-MB levels in cells. The direct targeting interactions among DLEU1, miR-23a-3p, and TNRC6A were verified through dual-luciferase reporter assay. Correlations between DLEU1, miR-23a-3p, and TNRC6A in serum samples from AMI patients were assessed by Pearson correlation analysis. In serum from AMI patients and hypoxia-treated H9c2 cells, the expression of DLEU1 and TNRC6A was upregulated, while the miR-23a-3p was downregulated. Functional experiments demonstrated that downregulating DLEU1 enhanced H9c2 cell viability, inhibited apoptosis, elevated SOD levels, and reduced MDA, LDH, and CK-MB levels under hypoxic conditions. Mechanistic studies confirmed that DLEU1 directly binds to miR-23a-3p, and inhibition of miR-23a-3p reversed the effects of downregulating DLEU1 on cardiomyocytes. Further studies identified that TNRC6A was a direct downstream target gene of miR-23a-3p. This study revealed that DLEU1 promotes myocardial cell apoptosis and exacerbates myocardial injury by adsorbing miR-23a-3p to upregulate TNRC6A during AMI. The results confirmed the role of the DLEU1/miR-23a-3p/TNRC6A axis in AMI pathogenesis, providing a novel potential therapeutic target for this disease.