Lactylation, a novel post-translational modification (PTM), in which a lactyl group, derived from lactate, is covalently added to lysine residues on the target proteins. Lactylation, first observed in histones in 2019, is increasingly recognized for its influence on gene expression, especially as it relates to shifts in cellular metabolism. ‘Metabolic reprogramming’ is one of the hallmarks of the myocardial infarction (MI), where cardiomyocytes shift from fatty acid oxidation to anaerobic glycolysis to meet energy demands, producing lactate. Very few studies suggest a positive correlation between increased lactate levels and mortality in heart failure patients, implying the importance of lactylation in the pathogenesis of MI. However, knowledge of lactylation post-MI is currently limited. The project aims to understand the differences in mitochondrial lactylated proteins and their relevance in the progression or restoration of MI pathogenesis. We also utilize AZD3965, a selective inhibitor of monocarboxylate transporter 1, which is responsible for bidirectional transport of lactate, to understand the lactylation profiling in MI.