Mustroph, Julian and Neef, Stefan and Maier, Lars S. (2017) CaMKII as a target for arrhythmia suppression. PHARMACOLOGY & THERAPEUTICS, 176. pp. 22-31. ISSN 0163-7258
Full text not available from this repository. (Request a copy)Abstract
Calcium/calmodulin-dependent protein kinase II (CaMKII) has emerged as key enzyme in many cardiac pathologies, especially heart failure (HF), myocardial infarction and cardiomyopathies, thus leading to contractile dysfunction and malignant arrhythmias. While many pathways leading to CaMKII activation have been elucidated in, recent years, hardly any clinically viable compounds affecting CaMKII activity have progressed from basic in vitro science to in vivo studies. This review focuses on recent advances in anti-arrhythmic strategies involving CaMKII. Specifically, both inhibition of CaMKII itself to prevent arrhythmias, as well as anti-arrhythmic approaches affecting CaMKII activity via alterations in signaling cascades upstream and downstream of CaMKII will be discussed. (C) 2016 Elsevier Inc. All rights reserved.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | CA2+/CALMODULIN-DEPENDENT PROTEIN-KINASE; POLYMORPHIC VENTRICULAR-TACHYCARDIA; SUDDEN CARDIAC DEATH; LONG-QT SYNDROME; RYANODINE RECEPTOR PHOSPHORYLATION; PAROXYSMAL ATRIAL-FIBRILLATION; BETA-ADRENERGIC STIMULATION; RETICULUM CA2+ LEAK; LATE SODIUM CURRENT; HEART-FAILURE; CaMKII; Arrhythmias; Inhibitors; Excitation-contraction coupling; Calcium leak |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Innere Medizin II |
| Depositing User: | Petra Gürster |
| Date Deposited: | 14 Dec 2018 13:16 |
| Last Modified: | 11 Sep 2020 08:26 |
| URI: | https://pred.uni-regensburg.de/id/eprint/1445 |
Actions (login required)
 |
View Item |
