Antagomir-21 Improve Post-MI Heart Failure by Inhibiting Myocardial Fibrosis and Myocardial Apoptosis

Abstract Background : Despite a significant improvement in the acute survival rate of myocardial infarction in recent decades, postischemic heart failure (HF) remains a common outcome (around 50%) and is a major cause of hospitalization and death. This study aimed to investigate whether antagomir-21 could ameliorate postischemic heart failure following persistent myocardial infarction, and to explore the underlying mechanism Methods ：mice were randomly divided into 3 groups: sham group, MI group, MI+antagomir-21 group. At four weeks post-myocardial infarction, we evaluated whether antagomir-21 could improve cardiac function by inhibiting myocardial fibrosis and apoptosis with experimental methods including cardiac ultrasound, Massone staining, WB, and TUNEL staining. Results : Results indicated that antagomir-21 decreased the expression of p-ERK1/2, caspase-3, caspase-8, TGF-β, Collagen I and Collagen III, thereby inhibiting excessive fibrosis and myocardial apoptosis in mice following persistent myocardial infarction.In mice experiments, antagomir-21 improved cardiac function, as evidenced by an increased ejection fraction and a reduced left ventricular end-diastolic diameter in the MI+antagomir-21 group compared to the MI group. Conclusions : Taken together, our findings suggest that antagomir-21 could alleviate postischemic heart failure by suppressing excessive fibrosis and myocardial apoptosis.