In METTL3-overexpressing H9c2 cells, SYD treatment reversed the hypertrophy induced by METTL3 overexpression.<h4>Conclusion</h4>SYD alleviates post-MI HF by regulating the mTOR/TFEB autophagy pathway through inhibition of METTL3-mediated m6A modification. The gene discussed is MTOR; the disease is myocardial infarction.