Indeed, in our study, Akt and also GSK-3β, which has been reported to specifically suppress cardiac fibroblast-mediated remodelling [39], were upregulated by exendin-4 after MI, at both total and phosphorylated protein level, suggesting that modulation of cardiomyocyte Akt/GSK-3β signalling plays a key role in mediating the chronic cardioprotective actions of GLP-1R activation and may thereby indirectly influence ECM remodelling. This evidence concerns the gene AKT1 and myocardial infarction.