Suppression of lncRNA attenuates myocardial infarction via / /ferroptosis axis.

Myocardial infarction (MI) is the leading cause of sudden death. Long non-doing RNAs (lncRNAs) were demonstrated to play crucial roles in multiple diseases, including cancer and cardiovascular diseases. Nevertheless, the molecular mechanism of lncNRAs in MI is unclear. In this study, we integrated bioinformatics and molecular biological experiments to identify the novel lncRNA transcripts and elucidated its regulatory mechanism in MI. First, we identified 10 dysregualted lncRNAs and found that lncRNA was the top risk factor in MI. Bioinformatics analysis predicted that lncRNA exerted function via targeting and was also the known regulator of ferroptosis. Inhibition or overexpression of lncRNA could regulate expression and downstream ferroptosis activity. Overexpression of could inhibit the expression of and the activity of ferroptosis, thereby attenuated cellular injury. Mechanically, co-transfection experiments showed that overexpression of could reverse the damage effect that was caused by lncRNA overexpression, via inhibiting and ferroptosis. Additionally, inhibition of lncRNA by stem cell membrane coated siRNA could attenuate MI in . Our study elucidated a novel mechanism containing lncRNA ///ferroptosis in MI, which provided a potential therapeutic for MI.Graphical Abstract. Stem cell membrane coated siRNA of lncRNA inhibits cardiomyocyte ferroptosis in myocardial infarction rat. Stem cell membrane-coated siRNA of lncRNA increases , and then suppresses the to reduce lipid peroxidation toxicity, and then inhibits cardiomyocyte ferroptosis. PUFA: polyunsaturated fatty acid.