Tumor necrosis factor-α mediates cardiac remodeling and ventricular dysfunction after pressure overload state

Circulation

Volumn 115, Issue 11, 2007, Pages 1398-1407

  Sun, Mei ^a   Chen, Manyin ^a   Dawood, Fayez ^a   Zurawska, Urszula ^a   Li, Jeff Y ^a   Parker, Thomas ^b   Kassiri, Zamaneh ^c   Kirshenbaum, Lorrie A ^d   Arnold, Malcolm ^e   Khokha, Rama ^c   Liu, Peter P ^a,f,g  

^a UNIVERSITY HEALTH NETWORK   (Canada)

^b ST MICHAEL'S HOSPITAL   (Canada)

^c UNIVERSITY OF TORONTO   (Canada)

^d UNIVERSITY OF MANITOBA   (Canada)

^e UNIVERSITY OF WESTERN ONTARIO   (Canada)

^f CANADIAN INSTITUTES OF HEALTH RESEARCH   (Canada)

^g TORONTO GENERAL HOSPITAL   (Canada)

Author keywords

Cardiomyopathy; Heart failure; Hypertension; Hypertrophy; Inflammation; Metalloproteinases; Remodeling

Indexed keywords

GELATINASE B; TUMOR NECROSIS FACTOR ALPHA; MESSENGER RNA;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; APOPTOSIS; ARTICLE; CONTROLLED STUDY; DESCENDING AORTA; ENZYME ACTIVITY; HEART VENTRICLE FUNCTION; HEART VENTRICLE HYPERTROPHY; INFLAMMATION; KNOCKOUT MOUSE; MALE; MOUSE; MOUSE STRAIN; NONHUMAN; PRIORITY JOURNAL; STATISTICAL SIGNIFICANCE; ANIMAL; AORTA; C57BL MOUSE; CELL CULTURE; CYTOLOGY; DISEASE MODEL; FIBROSIS; GENETICS; HEART LEFT VENTRICLE FUNCTION; HEART LEFT VENTRICLE HYPERTROPHY; HEART MUSCLE; HEART MUSCLE CELL; HEART VENTRICLE PRESSURE; HEART VENTRICLE REMODELING; IMMUNOLOGY; METABOLISM; MOUSE MUTANT; MYOCARDITIS; PATHOLOGY; PATHOPHYSIOLOGY; PHYSIOLOGY;

ANIMALS; AORTA; APOPTOSIS; CELLS, CULTURED; DISEASE MODELS, ANIMAL; FIBROSIS; HYPERTROPHY, LEFT VENTRICULAR; MALE; MATRIX METALLOPROTEINASE 9; MICE; MICE, INBRED C57BL; MICE, KNOCKOUT; MYOCARDITIS; MYOCARDIUM; MYOCYTES, CARDIAC; RNA, MESSENGER; TUMOR NECROSIS FACTOR-ALPHA; VENTRICULAR DYSFUNCTION, LEFT; VENTRICULAR PRESSURE; VENTRICULAR REMODELING;

EID: 34147098000     PISSN: 00097322     EISSN: None     Source Type: Journal    
DOI: 10.1161/CIRCULATIONAHA.106.643585     Document Type: Article

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