Calmodulin Kinase II, Sarcoplasmic Reticulum Ca2+ Leak, and Atrial Fibrillation

被引：38

作者：

Dobrev, Dobromir ^{[1
]}

Wehrens, Xander H. T. ^{[2
]}

机构：

[1] Tech Univ Dresden, Dept Pharmacol & Toxicol, D-01307 Dresden, Germany

[2] Baylor Coll Med, Dept Mol Physiol & Biophys & Med Cardiol, Houston, TX 77030 USA

来源：

TRENDS IN CARDIOVASCULAR MEDICINE | 2010年 / 20卷 / 01期

关键词：

INTRACELLULAR CALCIUM LEAK; RYANODINE RECEPTOR; CONTRACTILE DYSFUNCTION; MOLECULAR DETERMINANTS; RELEASE CHANNEL; PHOSPHORYLATION; HEART; MECHANISM; CAMKII; OVEREXPRESSION;

D O I：

10.1016/j.tcm.2010.03.004

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Although it is generally accepted that excitation-contraction coupling is defective in patients with atrial fibrillation, the underlying cellular mechanisms remain incompletely understood. Recent studies suggest that abnormal sarcoplasmic reticulum calcium "leak" via ryanodine receptors contributes to atrial arrhythmogenesis. Increased activity of the enzyme calmodulin kinase II (CaMKII) and, specifically, enhanced CaMKII phosphorylation of ryanodine receptors appear to play a critical role in the induction and perhaps maintenance of atrial fibrillation. In this review, we will summarize new insights into the role of enhanced CaMKI I in sarcoplasmic reticulum calcium leak and atrial arrhythmogenesis during atrial fibrillation. (Trends Cardiovasc Med 2010;20:30-34) (C) 2010, Elsevier Inc.

引用

页码：30 / 34

页数：5

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