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. 2021 Apr 30;129(1):98–113. doi: 10.1161/CIRCRESAHA.120.318402

Figure 8.

Figure 8.

Diabetes-induced delayed afterdepolarizations are dependent on CaMKIIδ (Ca2+/calmodulin-dependent protein kinase II)-S280 O-GlcNAcylation. A and B, delayed afterdepolarizations (DADs) and spontaneous action potentials (sAPs) were increased by high-glucose in streptozotocin (STZ)-treated wild type (WT; n=12 cells from 6 animals), but it was prevented in STZ-treated CaMKIIδ-S280A (n=18 cells from 6 animals). Nested t test. C and D, Diabetic hyperglycemia largely enhanced spontaneous diastolic activities, which were prevented by AIP (autocamtide-2-related inhibitory peptide), in CaMKIIδ-cKO and S280A but not in mutated Met281Val and Met282Val (MMVV). Additional Ang II (angiotensin II) treatment further enhanced the arrhythmogenic activities, which were prevented in CaMKIIδ-cKO and MMVV but not in S280A (n=total number of cells/animals is reported in the figure). Nested 1-way ANOVA, followed by Dunnett multiple comparisons test.