Apoptosis in severe, compensated pressure overload predominates in nonmyocytes and is related to the hypertrophy but not function

American Journal of Physiology - Heart and Circulatory Physiology

Volumn 300, Issue 3, 2011, Pages

  Gelpi, Ricardo J ^a,b   Park, Misun ^a   Gao, Shumin ^a   Dhar, Sunil ^a   Vatner, Dorothy E ^a   Vatner, Stephen F ^a  

^a RUTGERS NEW JERSEY MEDICAL SCHOOL   (United States)

^b UNIVERSIDAD DE BUENOS AIRES   (Argentina)

Author keywords

Heart failure; Left ventricular hypertrophy; Left ventricular wall stress; Programmed cell death

Indexed keywords

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; AORTA PRESSURE; APOPTOSIS; ARTICLE; BODY WEIGHT; CONTROLLED STUDY; DISEASE SEVERITY; HEART FAILURE; HEART LEFT VENTRICLE EJECTION FRACTION; HEART LEFT VENTRICLE ENDDIASTOLIC PRESSURE; HEART LEFT VENTRICLE FUNCTION; HEART LEFT VENTRICLE HYPERTROPHY; HEART LEFT VENTRICLE OVERLOAD; HEART LEFT VENTRICLE PRESSURE; HEART LEFT VENTRICLE WALL; HEART MUSCLE CELL; HEART RATE; MALE; MUSCLE STRESS; NONHUMAN; PRESSURE GRADIENT; PRIORITY JOURNAL; RAT; SYSTOLIC BLOOD PRESSURE;

ANIMALS; APOPTOSIS; DOGS; FEMALE; HEART FAILURE; HYPERTROPHY, LEFT VENTRICULAR; MALE; MYOCYTES, CARDIAC; RATS; RATS, SPRAGUE-DAWLEY; STROKE VOLUME; VENTRICULAR FUNCTION, LEFT;

EID: 79955065941     PISSN: 03636135     EISSN: 15221539     Source Type: Journal    
DOI: 10.1152/ajpheart.00998.2010     Document Type: Article

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