Abstract Background No human studies evaluating the efficacy of sodium glucose cotransporter 2 inhibitors (SGLT2-i) in preventing left ventricular dysfunction induced by anthracycline chemotherapy are available. Current evidence on this topic is based on few studies conducted on mouse models. Objective We investigated this issue through a meta-analysis of echocardiography studies that reported data on difference in left ventricular function between animals assuming SGLT2-i and controls in mouse models of anthracycline-induced cardiomyopathy. Methods The PubMed, OVID-MEDLINE and Cochrane library databases were systematically analysed to search English-language articles published from inception to 31 July 2022. Studies were identified by using Me-SH terms and crossing the following terms: “ sodium glucose cotransporter 2 inhibitors”, “gliflozin”, “anthracycline”, “cardiotoxicity”, “systolic dysfunction” and “echocardiography”. Results The meta-analysis included a total of 106 mice (Sprague Dawley and C57Bl/6 species) with anthracycline-induced cardiomyopathy from 7 studies, 60 mice assuming a SGLT2-i (Empagliflozin:4 studies, Dapagliflozin:2, Canagliflozin:1) and 46 controls. Compared with controls, left ventricle systolic function was significantly better in the pooled SGLT2-i group. Precisely, both fractional shortening (FS: 44,7±3,7 vs 32,6±3,3) and left ventricle ejection fraction (LVEF: 78,2±3,4 vs 64,2±4,9) were higher in the pooled SGLT2-i group than in the controls group, with standard mean difference (SMD) respectively being 2,42±0,56 for FS (CI: 1,326-3,510, p value <0.001) and 2,46±0,61 for LVEF (CI: 1,267-3,656, p value <0.001). Figure 1. Conclusions Our study shows a favourable effect of SGLT2-i in the prevention of left ventricular dysfunction induced by anthracycline chemotherapy in mouse models, suggesting that this pharmacological strategy should also be tested in clinical studies involving human subjects.