These results suggest that loss of LDHA in LDHA-cKO reduces the lactate concentration in myocardial tissue and downregulates α-MHC K1897 lactylation, which in turn reduces α-MHC–Titin interaction and exacerbates Ang II-induced heart failure, without obvious myocardial hypertrophy. The gene discussed is LDHA; the disease is cardiac hypertrophy.