Lkb1 knockout mouse develops spontaneous atrial fibrillation and provides mechanistic insights into human disease process

Journal of the American Heart Association

Volumn 4, Issue 3, 2015, Pages

  Ozcan, Cevher ^a,b   Battaglia, Emily ^a   Young, Rebeccah ^a   Suzuki, Gen ^a  

^a UNIVERSITY AT BUFFALO   (United States)

^b Pritzker School of Medicine   (United States)

Author keywords

Animal models of human disease remodeling; Atrial fibrillation; Atrium; Inflammation; Pathogenesis

Indexed keywords

AUTACOID; CONNEXIN 40; CONNEXIN 43; GAP JUNCTION PROTEIN; GJA1 PROTEIN, MOUSE; HYDROXYMETHYLGLUTARYL COENZYME A REDUCTASE KINASE; PROTEIN SERINE THREONINE KINASE; REACTIVE OXYGEN METABOLITE; STK11 PROTEIN, MOUSE;

AGE; ANIMAL; APOPTOSIS; ATRIAL FIBRILLATION; ATRIOVENTRICULAR BLOCK; BLOOD; C57BL MOUSE; CARDIAC MUSCLE CELL; CARDIOMYOPATHY; DEFICIENCY; DISEASE COURSE; ENZYMOLOGY; EXERCISE TOLERANCE; FIBROSIS; GENETICS; GENOTYPE; HEART ATRIUM FLUTTER; HEART FAILURE; HEART LEFT VENTRICLE FUNCTION; HEART RATE; HUMAN; KNOCKOUT MOUSE; MALE; METABOLISM; NECROSIS; PATHOLOGY; PATHOPHYSIOLOGY; PHENOTYPE;

AGE FACTORS; AMP-ACTIVATED PROTEIN KINASES; ANIMALS; APOPTOSIS; ATRIAL FIBRILLATION; ATRIAL FLUTTER; ATRIOVENTRICULAR BLOCK; CARDIOMYOPATHIES; CONNEXIN 43; CONNEXINS; DISEASE PROGRESSION; EXERCISE TOLERANCE; FIBROSIS; GENOTYPE; HEART FAILURE; HEART RATE; HUMANS; INFLAMMATION MEDIATORS; MALE; MICE, INBRED C57BL; MICE, KNOCKOUT; MYOCYTES, CARDIAC; NECROSIS; PHENOTYPE; PROTEIN-SERINE-THREONINE KINASES; REACTIVE OXYGEN SPECIES; VENTRICULAR DYSFUNCTION, LEFT; VENTRICULAR FUNCTION, LEFT;

EID: 84992243318     PISSN: None     EISSN: 20479980     Source Type: Journal    
DOI: 10.1161/JAHA.114.001733     Document Type: Article

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