Constitutively active MEK1 rescues cardiac dysfunction caused by over expressed GSK-3α during aging and hemodynamic pressure overload

American Journal of Physiology - Heart and Circulatory Physiology

Volumn 303, Issue 8, 2012, Pages

  Maejima, Yasuhiro ^a   Galeotti, Jonathan ^a   Molkentin, Jeffery D ^b   Sadoshima, Junichi ^a   Zhai, Peiyong ^a  

^a RUTGERS NEW JERSEY MEDICAL SCHOOL   (United States)

^b CINCINNATI CHILDREN'S HOSPITAL MEDICAL CENTER   (United States)

Author keywords

Apoptosis; Cardiac hypertrophy; Signal transduction

Indexed keywords

GLYCOGEN SYNTHASE KINASE 3ALPHA; MITOGEN ACTIVATED PROTEIN KINASE; MITOGEN ACTIVATED PROTEIN KINASE KINASE 1;

AGING; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; APOPTOSIS; ARTICLE; BODY WEIGHT; CELL SIZE; CONTROLLED STUDY; ENZYME PHOSPHORYLATION; HEART DISEASE; HEART LEFT VENTRICLE EJECTION FRACTION; HEART LEFT VENTRICLE OVERLOAD; HEART MUSCLE CELL; HEART MUSCLE FIBROSIS; HEART VENTRICLE HYPERTROPHY; MOUSE; NONHUMAN; PRIORITY JOURNAL; PROTEIN EXPRESSION; SHAM PROCEDURE; TIBIA; TRANSGENIC MOUSE;

AGING; ANIMALS; APOPTOSIS; CARDIOMEGALY; DISEASE MODELS, ANIMAL; ENZYME INHIBITORS; GLYCOGEN SYNTHASE KINASE 3; HEMODYNAMICS; MAP KINASE KINASE 1; MAP KINASE SIGNALING SYSTEM; MICE; MICE, TRANSGENIC; MYOCYTES, CARDIAC; SIGNAL TRANSDUCTION; STROKE VOLUME; VENTRICULAR DYSFUNCTION, LEFT; VENTRICULAR PRESSURE;

EID: 84867699737     PISSN: 03636135     EISSN: 15221539     Source Type: Journal    
DOI: 10.1152/ajpheart.00415.2012     Document Type: Article

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