Guo et al. [99] reported that in a transverse aortic constriction (TAC)-induced hypertrophy model, ACAA2 expression and its lactylation are significantly decreased, impairing fatty acid β-oxidation and mitochondrial oxidative phosphorylation, leading to metabolic dysfunction, pathological hypertrophy and worsened HF; while sodium lactate supplementation can restore ACAA2 lactylation, correct metabolic disturbance and alleviate hypertrophy, suggesting ACAA2 lactylation as a potential metabolic therapeutic target in HF. Here, ACAA2 is linked to hydrops fetalis.