Low-expressed GAS5 injure myocardial cells and progression of chronic heart failure via regulation of miR-223-3P.

Chronic heart failure (CHF) is a common disease in clinical practice, and its incidence has been increasing in recent years. Understanding the pathogenesis of CHF is the key to its future clinical diagnosis and treatment. Molecular research is a hot topic in modern hospitals, and long non-coding RNA (LncRNA) has been gradually understood and applied in many diseases. The situation of LncRNA GAS5 in CHF is still unclear, so this experiment will investigate the situation of GAS5 in CHF and its effect on myocardial cells, aiming to gain a preliminary understanding of the mechanism of GAS5's effect on CHF. In this study, the expression of GAS5 and miR-223-3p in peripheral blood of CHF patients and healthy subjects was first detected, GAS5 was low in CHF while miR-223-3p was high (P < 0.05). Subsequently, ROC curve analysis showed that GAS5 and miR-223-3p had good predictive value for the occurrence and recurrence of CHF. Secondly, through in vitro experiments, we found that inhibition of GAS5 with elevated expression of miR-223-3p decreased the proliferative capacity of cardiomyocytes and increased apoptotic capacity and inflammatory factors (P < 0.050). Through dual luciferase reporter and RNA immunoprecipitation experiment, we found that miR-223-3p was regulated by GAS5 in a targeted manner.

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