In primary cardiomyocyte ischemia models, OGT overexpression or the increase of O-GlcNAcylation with OGA inhibitors attenuates calcium overload, oxidative stress, and mitochondrial damage caused by oxidative injury (Ngoh et al., 2011), inhibits apoptosis, and has a protective effect on cardiomyocytes, whereas OGA overexpression exacerbates hypoxia and oxidative damage. Here, OGA is linked to ischemia.