BK Channel Dysfunction in Diabetic Coronary Artery: Role of the E3 Ubiquitin Ligases

被引：12

作者：

Qian, Ling-ling ^{[1
]}

Liu, Xiao-yu ^{[1
]}

Yu, Zhi-ming ^{[1
]}

Wang, Ru-xing ^{[1
]}

机构：

[1] Nanjing Med Univ, Dept Cardiol, Wuxi Peoples Hosp, Wuxi, Jiangsu, Peoples R China

来源：

FRONTIERS IN PHYSIOLOGY | 2020年 / 11卷

基金：

中国国家自然科学基金;

关键词：

diabetes mellitus; coronary artery; BK channel; ubiquitin-proteasome system; E3 ubiquitin ligase; CA2+-ACTIVATED K+ CHANNELS; BETA-1 SUBUNIT EXPRESSION; SMOOTH-MUSCLE-CELLS; LARGE-CONDUCTANCE; PROTEASOME SYSTEM; CA2+-DEPENDENT ACTIVATION; CARDIAC-HYPERTROPHY; ER STRESS; F-BOX; ATROGIN-1;

D O I：

10.3389/fphys.2020.00453

中图分类号：

Q4 [生理学];

学科分类号：

071003 ;

摘要：

Diabetic coronary arterial disease is a leading cause of morbidity and mortality in diabetic patients. The impaired function of large-conductance calcium-activated potassium channels (BK channels) is involved in diabetic coronary arterial disease. Many studies have indicated that the reduced BK channel expression in diabetic coronary artery is attributed to ubiquitin-mediated protein degradation by the ubiquitin-proteasome system. This review focuses on the influence and the mechanisms of BK channel regulation by E3 ubiquitin ligases in diabetic coronary arterial disease. Thus, BK channels regulated by E3 ubiquitin ligase may play a pivotal role in the coronary pathogenesis of diabetic mellitus and, as such, is a potentially attractive target for therapeutic intervention.

引用

页数：7

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