High Glucose Represses hERG K+ Channel Expression through Trafficking Inhibition | Zendy

Yuanqi Shi | Zendy; Meng Yan | Zendy; Lirong Liu | Zendy; Xiao Zhang | Zendy; Xue Wang | Zendy; Huaize Geng | Zendy; Xin Zhao | Zendy; Baoxin Li | Zendy

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High Glucose Represses hERG K+ Channel Expression through Trafficking Inhibition

Author(s) -

Yuanqi Shi,

Meng Yan,

Lirong Liu,

Xiao Zhang,

Xue Wang,

Huaize Geng,

Xin Zhao,

Baoxin Li

Publication year - 2015

Publication title -

cellular physiology and biochemistry

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.486

H-Index - 87

eISSN - 1421-9778

pISSN - 1015-8987

DOI - 10.1159/000430353

Subject(s) - herg , potassium channel , microbiology and biotechnology , chemistry , pharmacology , biology , medicine , endocrinology

Abnormal QT prolongation is the most prominent cardiac electrical disturbance in patients with diabetes mellitus (DM). It is well known that the human ether-ago-go-related gene (hERG) controls the rapid delayed rectifier K+ current (IKr) in cardiac cells. The expression of the hERG channel is severely down-regulated in diabetic hearts, and this down-regulation is a critical contributor to the slowing of repolarization and QT prolongation. However, the intracellular mechanisms underlying the diabetes-induced hERG deficiency remain unknown.

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