Non-ion channel therapeutics for heart failure and atrial fibrillation: Are CaMKII inhibitors ready for clinical use?

被引：10

作者：

Grandi, Eleonora ^{[1
]}

Dobrev, Dobromir ^{[2
]}

机构：

[1] Univ Calif Davis, Dept Pharmacol, 451 Hlth Sci Dr,Tupper Hall Rm 2427, Davis, CA 95616 USA

[2] Univ Duisburg Essen, West German Heart & Vasc Ctr, Inst Pharmacol, Hufelandstr 55, D-45122 Essen, Germany

来源：

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY | 2018年 / 121卷

基金：

美国国家卫生研究院;

关键词：

CaMKII; Heart failure; Atrial fibrillation; Arrhythmia; Small molecules; PROTEIN-KINASE-II; SR CA2+ LEAK; CARDIAC-HYPERTROPHY; K+ CURRENT; ISOFORM; ARRHYTHMOGENESIS; PHOSPHORYLATION; CONTRACTILE; DYSFUNCTION; ACTIVATION;

D O I：

10.1016/j.yjmcc.2017.10.010

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

The Ca2+-calmodulin dependent protein kinase II (CaMKII) is an established central mediator of electro-physiological and contractile responses to cardiac stress, and its hyper-activation in cardiac diseases has been linked to heart failure (HF) and arrhythmia. Here we summarize the evidence supporting the role of CaMKII as a critical nodal point for therapeutic intervention against HF and atrial and ventricular tachyarrhythmias. Targeting of CaMKII in heart with inhibitors possessing appropriate selectivity might represent a novel therapeutic approach for HF and arrhythmias.

引用

页码：300 / 303

页数：4

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