We demonstrated that this short-term and mild diabetes-induced cardioprotection may be, at least in part, due to an increased transcriptional expression of markers of antioxidant defense and the prosurvival PI3K/Akt pathway and due to the downregulation of apoptotic genes, proinflammatory cytokine tumor necrosis factor-α, profibrogenic transforming growth factor-β, and hypertrophic marker alpha actin-1. Here, ACTA1 is linked to diabetes mellitus.