Long noncoding RNAs (lncRNAs) have been considered as crucial regulators of acute myocardial infarction (AMI).In this study,to analyze the effect of differentiation antagonizing nonprotein cod-ing RNA (DANCR) of lncRNA on cardiomyocyte damage in AMI,cardiomyocyte injury was induced by oxygen-glucose deprivation (OGD).Cell counting kit-8 (CCK-8) assay and flow cytometry were used to assess cell viability and apoptosis,respectively.Quantitative real-time PCR was used to measure the expression levels of DANCR and miR-19a-3p.Bioinformatics analysis and luciferase gene reporter assay were utilized to explore the relationship among DANCR,miR-19a-3p,and mitogen-activated protein kinase 1 (MAPK1).CCK-8 and TUNELassays were used to explore the effects of DANCR alone or plus miR-19a-3p on the viability and apoptosis of OGD/R-exposed HL-1 cells.Western blot analysis was used to detect changes in the MAPK1/ERK1/2 pathway in HL-1 cells.We found that DANCR expression and miR-19a-3p level are negatively correlated as DANCR expres-sion is increased,while miR-19a-3p level is decreased in AMI patients\' serum and OGD/R-exposed HL-1 cells.DANCR knockdown increased miR-19a-3p level,and miR-19a-3p inhibition increased DANCR expression.Moreover,DANCR directly binds to miR-19a-3p.DANCR knockdown reduced viability but induced apoptosis in OGD/R-exposed HL-1 cells,while miR-19a-3p inhibition weakens these effects.Furthermore,MAPK1 is a target of miR-19a-3p.miR-19a-3p overexpression decreases MAPK1 and ERK1/2 in HL-1 cells,while miR-19a-3p inhibition increases MAPK1 and ERK1/2 in HL-1 cells.Moreover,DANCR knockdown reduces myocardium apoptosis in mice with the left anterior descending artery ligated.DANCR knockdown effectively restores myocardial cell apoptosis by regulating the miR-19a-3p/MAPK1/ERK1/2 axis.