Knockdown of lncRNA RMST protect against myocardial infarction through regulating miR-5692 and MAGI3 axis

Myocardial infarction is the leading cause of death worldwide. The aim of this study was to investigate the function and mechanism of lncRNA RMST in myocardial infarction.

H/R and H₂O₂ models were established to assess the function of lncRNA RMST in vitro. Mouse myocardial infarction was used to analyze the function of lncRNA RMST in vivo. Bioinformatics analysis was performed to predict the potential binding target of lncRNA RMST. Rescue experiments were performed to verify the relationship between RMST and its target.

The expression of lncRNA RMST was significantly increased with H/R or H₂O₂ treatment. Knockdown of lncRNA RMST improved cell death and protected mitochondria from H/R injury in vitro. In vivo, cardiac function was significantly attenuated by knockdown of lncRNA RMST. We also provided evidence that miR-5692 was a direct target of lncRNA RMST. Rescue experiments showed that knockdown of miR-5692 could restore the function of RMST.

Our study is the first to prove the function and mechanism of lncRNA RMST in myocardial infarction. Thus, a deeper understanding of the role of lncRNA RMST in myocardial infarction may provide new insights for the clinical intervention of MI.