Diastolic dysfunction and arrhythmias caused by overexpression of CaMKIIδC can be reversed by inhibition of late Na+ current

Basic Research in Cardiology

Volumn 106, Issue 2, 2011, Pages 263-272

  Sossalla, Samuel ^a   Maurer, Ulrike ^a   Schotola, Hanna ^a   Hartmann, Nico ^a   Didié, Michael ^a   Zimmermann, Wolfram H ^a   Jacobshagen, Claudius ^a   Wagner, Stefan ^a   Maier, Lars S ^a  

^a UNIVERSITY OF GÖTTINGEN   (Germany)

Author keywords

Arrhythmias; CaMKII; Contractility; Diastolic dysfunction; Excitation contraction coupling; Heart failure

Indexed keywords

CALCIUM CALMODULIN DEPENDENT PROTEIN KINASE II; RANOLAZINE; CALCIUM; SARCOPLASMIC RETICULUM CALCIUM TRANSPORTING ADENOSINE TRIPHOSPHATASE; SODIUM; SODIUM CALCIUM EXCHANGE PROTEIN;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARRHYTHMOGENESIS; ARTICLE; CONTROLLED STUDY; DIASTOLE; DIASTOLIC DYSFUNCTION; ECHOCARDIOGRAPHY; EXCITATION CONTRACTION COUPLING; GENE OVEREXPRESSION; HEART ARRHYTHMIA; HEART CONTRACTION; HEART EJECTION FRACTION; HEART MUSCLE CELL; HEART MUSCLE TENSION; HEART PAPILLARY MUSCLE; MOUSE; MUSCLE ISOMETRIC CONTRACTION; MUSCLE TWITCH; NONHUMAN; PATHOPHYSIOLOGY; SODIUM CURRENT; TRANSGENIC MOUSE; ANIMAL; DIASTOLIC HEART FAILURE; ENZYMOLOGY; HEART MUSCLE; METABOLISM; PATHOLOGY; PHENOTYPE;

ANIMALS; ARRHYTHMIAS, CARDIAC; CALCIUM; CALCIUM-CALMODULIN-DEPENDENT PROTEIN KINASE TYPE 2; HEART FAILURE, DIASTOLIC; MICE; MICE, TRANSGENIC; MYOCARDIAL CONTRACTION; MYOCARDIUM; PAPILLARY MUSCLES; PHENOTYPE; SARCOPLASMIC RETICULUM CALCIUM-TRANSPORTING ATPASES; SODIUM; SODIUM-CALCIUM EXCHANGER;

EID: 79957795565     PISSN: 03008428     EISSN: 14351803     Source Type: Journal    
DOI: 10.1007/s00395-010-0136-x     Document Type: Article

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