METTL3 and Myocardial fibrosis: Our study also observed dynamic changes in METTL3 and ALKBH5 expression during myocardial fibrosis post‐myocardial infarction and in the proliferation and differentiation of hypoxic‐induced cardiac fibroblasts, suggesting that a compensatory mechanism involving METTL3 and ALKBH5 may also exist in the proliferation and differentiation of cardiac fibroblasts, albeit this hypothesis warrants further experimental validation in the future.