New antiarrhythmic targets to control intracellular calcium handling

被引:26
作者
Driessen, H. E. [1 ]
Bourgonje, V. J. A. [1 ]
van Veen, T. A. B. [1 ]
Vos, M. A. [1 ]
机构
[1] Univ Med Ctr Utrecht, Dept Med Physiol, Div Heart & Lungs, NL-3584 CM Utrecht, Netherlands
关键词
Arrhythmia; Calcium; Drugs; Treatment; PROTEIN-KINASE-II; TORSADES-DE-POINTES; LATE SODIUM CURRENT; POLYMORPHIC VENTRICULAR-TACHYCARDIA; RYANODINE RECEPTOR; NA+/CA2+ EXCHANGER; IN-VIVO; CARDIOPROTECTIVE DRUG; ANTIANGINAL AGENT; NA/CA EXCHANGE;
D O I
10.1007/s12471-014-0549-5
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Sudden cardiac death due to ventricular arrhythmias is a major problem. Drug therapies to prevent SCD do not provide satisfying results, leading to the demand for new antiarrhythmic strategies. New targets include Ca2+/Calmodulin-dependent protein kinase II (CaMKII), the Na/Ca exchanger (NCX), the Ryanodine receptor (RyR, and its associated protein FKBP12.6 (Calstabin)) and the late component of the sodiumcurrent (INa-Late), all related to intracellular calcium (Ca2+) handling. In this review, drugs interfering with these targets (SEA-0400, K201, KN-93, W7, ranolazine, sophocarpine, and GS-967) are evaluated and their future as clinical compounds is considered. These new targets prove to be interesting; however more insight into long-term drug effects is necessary before clinical applicability becomes reality.
引用
收藏
页码:198 / 213
页数:16
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