CaMKII activation via S280 O-GlcNAcylation regulates IK1 and Ito recovery in hyperglycemia. a Representative voltage-gated K+ currents and IK1 traces in normoglycemia and hyperglycemia in CaMKIIδ-knockout (KO), overexpression (OE) and O-GlcNAc-resistant S280A knock-in mouse myocytes. b–j K+ current remodeling in CaMKIIδ-KO and OE in normoglycemia. CaMKIIδ-S280A had a normal baseline phenotype. Hyperglycemia effects on Ito recovery kinetics (f, g) and IK1 (h, i) but not on Ito amplitude (b) were prevented in both CaMKIIδ-KO and S280A. Two-way ANOVA; *p < 0.05, **p < 0.01, ***p < 0.001 vs. normoglycemia; †p < 0.05, ††p < 0.01, †††p < 0.001 vs. WT control