| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 8662120 | International Journal of Cardiology | 2018 | 34 Pages |
Abstract
Our data suggested that hyperglycemia increased the O-GlcNAc modification of Nav1.5 expression and decreased the interaction between Nav1.5 and Nedd4-2/SAP-97, which led to the abnormal expression and distribution of Nav1.5, loss of function of the sodium channel, and prolongation of the PR/QT interval. Excessive O-GlcNAc modification of Nav1.5 is a novel signaling event, which may be an underlying contributing factor for the development of the arrhythmogenesis in DH.
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Authors
Peng Yu, Lili Hu, Jinyan Xie, Sisi Chen, Lin Huang, Zixuan Xu, Xiao Liu, Qiongqiong Zhou, Ping Yuan, Xia Yan, Jiejin Jin, Yang Shen, Wengen Zhu, Linghua Fu, Qi Chen, Jianhua Yu, Jianxin Hu, Qing Cao, Kui Hong,