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. Author manuscript; available in PMC: 2021 Jun 23.
Published in final edited form as: Circ Res. 2021 Apr 30;129(1):98–113. doi: 10.1161/CIRCRESAHA.120.318402

Figure 7. Diabetes-induced arrhythmogenic action potential remodeling is dependent predominantly on CaMKIIδ-S280 O-GlcNAcylation.

Figure 7.

A, APD prolongation and alternans in STZ-treated WT murine ventricular myocytes (n=16 cells from 7 animals). B, Arrhythmogenic AP remodeling in STZ was abolished by AIP (n=11 cells from 4 animals). C, APD prolongation was prevented in STZ-treated CaMKIIδ-S280A (n=22 cells from 6 animals). D, APD prolongation and alternans in STZ-treated CaMKIIδ-MMVV (n=17 cells from 6 animals). Nested t-test. E-F, AP remodeling was CaMKII-dependent and involved both hyperglycemia-dependent S280 O-GlcNAcylation (predominant mechanism) and Ang-II-dependent 281/2MM oxidation (n=total number of cells/animals is reported in the figure). Nested one-way ANOVA, followed by Dunnett’s multiple comparisons test.