Objective：To determine the effect and mechanisms of monocarboxylate transporter 1(MCT1)-mediated mitochondrial lactate shuttle on ventricular remodeling and heart failure induced by transverse aortic constriction(TAC) in mice.Methods：An animal model of cardiac hypertrophy was created by TAC in male C57BL/6 mice.Cardiac dimensions and functions were evaluated by echocardiography after 2 weeks，4 weeks， and 8 weeks following TAC，respectively.There were four groups：①Sham-operate group；②TAC 2 weeks group；③TAC 4 weeks group；④TAC 8 weeks group.Intracellular lactate and malondialdehyde(MDA)were measured by colorimetric，the proteins expression of cleaved-caspase 3 and MCT1 were detected by Western blot.Results：As echocardiography evaluation，the mice exhibited cardiac hypertrophy after TAC 2 weeks，heart failure after TAC 4 weeks，and severe heart failure after TAC 8 weeks.An increasing gradient of lactate and MDA concentrations，as well as cleaved-caspase 3 and MCT1 protein expressions were identified in the sham，TAC 2 weeks，and TAC 4 and 8 weeks groups.Besides，the concentrations of lactate and MDA and expressions of cleaved-caspase 3 and MCT1 were also found higher in the TAC 4 and 8 weeks groups than those of the sham and TAC 2 weeks groups.Conclusions：MCT1-mediated mitochondrial lactate shuttle plays an important role in the development of myocardial remodeling and heart failure.The molecular mechanisms may be through inducing oxidative stress and activating mitochondrial control of apoptosis.