Cardiomyocyte-specific deletion of Gsk3α mitigates post-myocardial infarction remodeling, contractile dysfunction, and heart failure

Journal of the American College of Cardiology

Volumn 64, Issue 7, 2014, Pages 696-706

  Ahmad, Firdos ^a,b   Lal, Hind ^a,b   Zhou, Jibin ^a   Vagnozzi, Ronald J ^a   Yu, Justine E ^a   Shang, Xiying ^a   Woodgett, James R ^c   Gao, Erhe ^a   Force, Thomas ^a,b  

^a TEMPLE UNIVERSITY SCHOOL OF MEDICINE   (United States)

^b VANDERBILT UNIVERSITY   (United States)

^c MOUNT SINAI HOSPITAL   (Canada)

Author keywords

cardiomyocyte proliferation; GSK 3 ; heart failure; myocardial infarction; ventricular remodeling

Indexed keywords

CARDIOMYOCYTE PROLIFERATION; GSK-3Α; HEART FAILURE; MYOCARDIAL INFARCTION; VENTRICULAR REMODELING;

ANIMALS; APOPTOSIS; CELL PROLIFERATION; DISEASE MODELS, ANIMAL; DNA; GENE DELETION; GLYCOGEN SYNTHASE KINASE 3; HEART FAILURE; IMMUNOHISTOCHEMISTRY; IN SITU NICK-END LABELING; MALE; MICE; MICE, INBRED C57BL; MYOCARDIAL CONTRACTION; MYOCARDIAL INFARCTION; MYOCYTES, CARDIAC; VENTRICULAR DYSFUNCTION, LEFT; VENTRICULAR REMODELING;

EID: 84905995337     PISSN: 07351097     EISSN: 15583597     Source Type: Journal    
DOI: 10.1016/j.jacc.2014.04.068     Document Type: Article

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