A novel role for tumor necrosis factor-like weak inducer of apoptosis (tweak) in the development of cardiac dysfunction and failure

Circulation

Volumn 119, Issue 15, 2009, Pages 2058-2068

  Jain, Mohit ^a   Jakubowski, Aniela ^b   Cui, Lei ^a   Shi, Jianru ^a   Su, Lihe ^b   Bauer, Michael ^a   Guan, Jian ^a,c   Lim, Chee Chew ^d,e   Naito, Yoshiro ^a,f   Thompson, Jeffrey S ^b   Sam, Flora ^c   Ambrose, Christine ^b   Parr, Michael ^b,g   Crowell, Thomas ^b   Lincecum, John M ^b,d   Wang, Monica Z ^b,h   Hsu, Yen Ming ^b   Zheng, Timothy S ^b   Michaelson, Jennifer S ^b,h   Liao, Ronglih ^a,i   Burkly, Linda C ^b   more..

^a BRIGHAM AND WOMEN S HOSPITAL   (United States)

^b BIOGEN   (United States)

^c BOSTON UNIVERSITY SCHOOL OF MEDICINE   (United States)

^d School of Medicine ^*

^e VANDERBILT UNIVERSITY SCHOOL OF MEDICINE   (United States)

^f HYOGO COLLEGE OF MEDICINE   (Japan)

^g ALS Therapy Development Institute   (Canada)

^h ALS Therapy Development Institute   (United States)

ⁱ HARVARD MEDICAL SCHOOL   (United States)

Author keywords

Cardiomyocytes; Fn14 TWEAK receptorm; Heart failure; Hypertrophy; Mouse; Tweak protein

Indexed keywords

ACETYLSALICYLIC ACID; ANGIOTENSIN RECEPTOR ANTAGONIST; BETA ADRENERGIC RECEPTOR BLOCKING AGENT; DIGOXIN; DIPEPTIDYL CARBOXYPEPTIDASE INHIBITOR; DIURETIC AGENT; HYDRALAZINE; HYDROXYMETHYLGLUTARYL COENZYME A REDUCTASE INHIBITOR; NITRATE; SPIRONOLACTONE; TUMOR NECROSIS FACTOR; TUMOR NECROSIS FACTOR ALPHA; TUMOR NECROSIS FACTOR LIKE WEAK INDUCER OF APOPTOSIS; TUMOR NECROSIS FACTOR LIKE WEAK INDUCER OF APOPTOSIS RECEPTOR; TUMOR NECROSIS FACTOR RECEPTOR; UNCLASSIFIED DRUG; WARFARIN; HYBRID PROTEIN; TNFSF12 PROTEIN, HUMAN; TNFSF12 PROTEIN, MOUSE; TWEAK RECEPTOR;

ADENOVIRUS; ADULT; AGED; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL TISSUE; APOPTOSIS; ARTICLE; CARDIAC PATIENT; CELL ELONGATION; CONGESTIVE CARDIOMYOPATHY; CONTROLLED STUDY; DISEASE SEVERITY; FEMALE; GENE EXPRESSION; HEART DISEASE; HEART FAILURE; HEART MUSCLE CELL; HEART MUSCLE FIBROSIS; HUMAN; HUMAN CELL; MAJOR CLINICAL STUDY; MALE; MOUSE; NONHUMAN; NUCLEOTIDE SEQUENCE; PATHOGENESIS; PHENOTYPE; PRIORITY JOURNAL; PROTEIN EXPRESSION; SIGNAL TRANSDUCTION; TRANSGENE; UPREGULATION; ANIMAL; BLOOD; C57BL MOUSE; CARDIOMYOPATHY; CELL SIZE; CORONARY ARTERY DISEASE; DBA MOUSE; FIBROSIS; GENETIC TRANSDUCTION; GENETICS; HYPERTENSION; METABOLISM; MIDDLE AGED; PATHOLOGY; PHYSIOLOGY; TRANSGENIC MOUSE;

ANIMALS; APOPTOSIS; CARDIOMYOPATHIES; CARDIOMYOPATHY, DILATED; CELL SIZE; CORONARY DISEASE; FEMALE; FIBROSIS; HEART FAILURE; HUMANS; HYPERTENSION; MALE; MICE; MICE, INBRED C57BL; MICE, INBRED DBA; MICE, TRANSGENIC; MIDDLE AGED; MYOCYTES, CARDIAC; PHENOTYPE; RECEPTORS, TUMOR NECROSIS FACTOR; RECOMBINANT FUSION PROTEINS; TRANSDUCTION, GENETIC; TUMOR NECROSIS FACTORS;

EID: 65449164651     PISSN: 00097322     EISSN: 15244539     Source Type: Journal    
DOI: 10.1161/CIRCULATIONAHA.108.837286     Document Type: Article

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