Notably, there were no significant differences in cardiomyocyte-specific glucose transporter 4, glycolysis, or glucose uptake among aged WT mice, Y-Sesn2 KO mice, and young WT mice that had been subjected to pressure overload-induced cardiac hypertrophy; however, glucose oxidation was significantly lower in aged WT mice and in Y-Sesn2 KO mice than in young WT mice, due to the reduction of mitochondrial function. Here, SESN2 is linked to cardiac hypertrophy.