ROS in diabetic atria regulate SK2 degradation by Atrogin-1 through the NF-κB signaling pathway.

One of the independent risk factors for atrial fibrillation (AF) is diabetes mellitus (DM); however, the underlying mechanisms causing AF in DM are unknown. Our previous investigation indicated that the muscle-specific E3 ligase Atrogin-1 contributes to SK2 protein degradation in the atria of streptozotocin (STZ)-induced DM mice, increasing susceptibility to atrial arrhythmias. However, the underlying mechanism of Atrogin-1-mediated SK2 degradation and associated signaling pathways are unclear. The aim of this study was to elucidate the relationship among ROS, the NF-κB signaling pathway, and Atrogin-1 protein expression in the atrial myocardia of DM mice. We found that SK2 expression was downregulated comitant with increased reactive oxygen species (ROS) generation and enhanced NF-κB signaling activation in the atrial cardiomyocytes of DM mice. These observations were mimicked by exogenously applicating H

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Déclaration de conflit d'intérêts

Declaration of interests The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. Jian Xu and Dong Zhang, designed experiments and wrote the first draft of the manuscript. YiBo Ma, Yi Zhang, Hui Du, WenPing Luo and Ruxing Wang, provided important intellectual content. Fu Yi provided financial support and revised the manuscript. All authors critically reviewed, interpreted the data and approved the final version of the manuscript.