title: Experimental antiarrhythmic targets: CaMKII inhibition - ready for clinical evaluation?
abstract: In the recent years, Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) was suggested to be associated with cardiac hypertrophy and heart failure but also with arrhythmias both in animal models as well as in the human heart. This article focuses on the role of CaMKII for excitation-contraction coupling but more explicitly it highlights major CaMKIIdependent proarrhythmogenic mechanisms including SR Ca(2+) leak and late Na(+) current. Because a clinical significance of CaMKII is implied for both mechanisms, CaMKII inhibition is suggested to be a therapeutical approach in the near future.
authors.affiliation: Abt. Kardiologie und Pneumologie / Herzzentrum, Deutsches Zentrum fur Herzkreislaufforschung, Georg-August-Universitat Gottingen, Robert-Koch-Str. 40 37075 Gottingen, Germany. lmaier@med.uni-goettingen.de.
authors.forename: Lars S
authors.initials: LS
authors.lastname: Maier
mesh_terms: D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use*; D001145:Arrhythmias, Cardiac / Q000188:drug therapy / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2 / Q000037:antagonists & inhibitors*; D006801:Humans; D011188:Potassium / Q000378:metabolism; D047428:Protein Kinase Inhibitors / Q000627:therapeutic use*
chemical_list: D000889:Anti-Arrhythmia Agents; D047428:Protein Kinase Inhibitors; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D011188:Potassium; D002118:Calcium