LncRNA HOXA11-AS Promotes Myocardial Injury in Chronic Heart Failure by Sponging miR-342-3p

Objective LncRNA HOXA11-AS was abnormally upregulated during heart failure, suggesting that it might be involved in the development of chronic heart failure (CHF). This study aims to explore the diagnostic value of HOXA11-AS in CHF and its mechanism of action in myocardial injury. Methods The level of HOXA11-AS in serum was detected by real-time quantitative polymerase chain reaction (RT-qPCR), and its diagnostic efficacy was evaluated by ROC curve. The model of CHF was established by treating AC16 cells with doxorubicin (DOX). Cell viability and apoptosis were detected by cell counting kit-8 (CCK-8) and flow cytometry. The levels of inflammatory factors and myocardial injury markers were detected by enzyme-linked immunosorbent assay (ELISA). The content of malondialdehyde (MDA) and the activity of superoxide dismutase (SOD) were detected by kits. Dual-luciferase reporter assay was used to verify the targeting relationship between HOXA11-AS and miR-342-3p. Results The expression of HOXA11-AS in the serum of CHF patients was significantly increased. ROC analysis showed that HOXA11-AS had a high diagnostic value for CHF. In the DOX-induced cell model, knocking down HOXA11-AS could significantly enhance cell viability, inhibit cell apoptosis, and reduce the release of myocardial injury markers, pro-inflammatory factors, as well as the level of oxidative stress. miR-342-3p was the target gene of HOXA11-AS. Inhibition of miR-342-3p could reverse the myocardial protective effect produced by the knockout of HOXA11-AS. Conclusion HOXA11-AS, as a potential biomarker for diagnosing CHF, exacerbates myocardial injury, inflammatory response and oxidative stress by sponging miR-342-3p.