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Oxidized CaMKII and O-GlcNAcylation cause increased atrial fibrillation in diabetic mice by distinct mechanisms

Mesubi, Olurotimi O. ; Rokita, Adam G. ; Abrol, Neha ; Wu, Yuejin ; Chen, Biyi ; Wang, Qinchuan ; Granger, Jonathan M. ; Tucker-Bartley, Anthony ; Luczak, Elizabeth D. ; Murphy, Kevin R. ; Umapathi, Priya ; Banerjee, Partha S. ; Boronina, Tatiana N. ; Cole, Robert N. ; Maier, Lars S. ; Wehrens, Xander H. ; Pomerantz, Joel L. ; Song, Long-Sheng ; Ahima, Rexford S. ; Hart, Gerald W. ; Zachara, Natasha E. ; Anderson, Mark E.



Abstract

Diabetes mellitus (DM) and atrial fibrillation (AF) are major unsolved public health problems, and diabetes is an independent risk factor for AF. However, the mechanism(s) underlying this clinical association is unknown. ROS and protein O-GlcNAcylation (OGN) are increased in diabetic hearts, and calmodulin kinase II (CaMKII) is a proarrhythmic signal that may be activated by ROS (oxidized CaMKII, ...

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