Abstract: Objective: To explore the mechanism and new therapeutic targets of anthracycline-induced cardiotoxicity.Methods: A total of 106 cases of breast cancer patients were divided into cardiac dysfunction group and control group based on echocardiography to identify cancer therapeutics-related cardiac functional impairment.Differentially expressed miRNAs between the two groups were screened out by high-throughput microarray technology.The model of H9C2 myocardial cell damage induced by anthracyclines was constructed in vitro, and the role of miR-25a-5p in the H9C2 myocardial cell damage induced by anthracyclines was observed by regulating the expression of miR-25a-5p.Results: Cancer therapeutics-related cardiac dysfunction occurred in 9 breast cancer patients, and a total of 9 differentially expressed miRNAs were identified between the two groups.Eight of these miRNAs were further validated in vitro model, especially miR-25a-5p.Up-regulation of miR-25a-5p could further aggravate the anthracycline-induced oxidative damage in myocardial cells.Conclusion: The miR-25a-5p aggravates anthracycline-induced myocardial damage and may be a new biomarker and therapeutic target.