Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

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

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2021 The Authors.

Circulation Research is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial-NoDerivs License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited, the use is noncommercial, and no modifications or adaptations are made.

This article is made available via the PMC Open Access Subset for unrestricted re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the COVID-19 pandemic or until permissions are revoked in writing. Upon expiration of these permissions, PMC is granted a perpetual license to make this article available via PMC and Europe PMC, consistent with existing copyright protections.

PMC Copyright notice

Figure 7. — Diabetes-induced arrhythmogenic action potential remodeling is dependent predominantly on CaMKIIδ (Ca²⁺/calmodulin-dependent protein kinase II)-S280 O-GlcNAcylation. A, Action potential duration (APD) prolongation and alternans in streptozotocin (STZ)-treated wild-type (WT) murine ventricular myocytes (n=16 cells from 7 animals). B, Arrhythmogenic action potential (AP) remodeling in STZ was abolished by AIP (autocamtide-2-related inhibitory peptide; 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-mutated Met281Val and Met282Val (MMVV; n=17 cells from 6 animals). Nested t test. E and 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 1 way ANOVA, followed by Dunnett multiple comparisons test. CaSpF indicates Ca²⁺ spark frequency.