Abstract
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.
Highlights
Specialty section: This article was submitted to Vascular Physiology, a section of the journal Frontiers in Physiology
This review focuses on the influence and the mechanisms of BK channel regulation by E3 ubiquitin ligases in diabetic coronary arterial disease
An increasing body of evidence suggests that large-conductance calcium-activated potassium channels (BK channels) in coronary arterial smooth muscle cells (CASMCs) play an important role in diabetic coronary arterial disease (Wang et al, 2012a; Yi et al, 2014)
Summary
Specialty section: This article was submitted to Vascular Physiology, a section of the journal Frontiers in Physiology. 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.
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