Sestrin2 Protein Modulates Pyroptosis of Human Coronary Artery Endothelial Cells by Binding to MiR-3160-5p

Background Cardiovascular diseases (CVDs) caused by atherosclerosis (AS) are the leading cause of death and a major health concern globally. However, the mechanisms that lead to have not been fully elucidated. Sestrin2 protein plays an important protective role in myocardial I/R by inhibiting cell apoptosis and other pathways. The aim of this study was to explore the role of Sestrin2 protein in modulating pyroptosis in human coronary artery endothelial cells and explore the specific mechanism of this function. Experimental methods H ₂ O ₂ was used to establish a pyroptosis model. The expression levels of Sestrin2 protein and mir-3160-5p in the HCAECs pyroptosis model were determined. The impact on the apoptosis of HCAECs was clarified by regulating the expression level of mir-3160-5p. The regulatory relationship between Sestrin2 protein and mir-3160-5p was explored in the pyroptosis model. Conclusion The findings showed that Sestrin2 protein inhibited H ₂ O ₂ -induced pyroptosis of HCAECs and inhibited miR-3160-5p expression, indicating that Sestrin2 protein inhibited H ₂ O ₂ -induced pyroptosis of HCAECs by binding to miR-3160-5p.