Glucose transporter 4-deficient hearts develop maladaptive hypertrophy in response to physiological or pathological stresses

American Journal of Physiology - Heart and Circulatory Physiology

Volumn 313, Issue 6, 2017, Pages H1098-H1108

  Wende, Adam R ^a,b   Kim, Jaetaek ^a   Holland, William L ^a   Wayment, Benjamin E ^a   O’Neill, Brian T ^a,c   Tuinei, Joseph ^a   Brahma, Manoja K ^b   Pepin, Mark E ^b   McCrory, Mark A ^b   Luptak, Ivan ^d   Halade, Ganesh V ^e   Litwin, Sheldon E ^a   Abel, E Dale ^a,c  

^a UNIVERSITY OF UTAH SCHOOL OF MEDICINE   (United States)

^b University of Alabama at Birmingham   (United States)

^c UNIVERSITY OF IOWA   (United States)

^d BOSTON UNIVERSITY SCHOOL OF MEDICINE   (United States)

^e University of Alabama at Birmingham and Birmingham Veterans Affairs Medical Center   (United States)

Author keywords

Cardiac hypertrophy; Exercise training; Glucose metabolism; Heart failure; Mitochondrial metabolism; Pressure overloadz

Indexed keywords

3 HYDROXYACYL COENZYME A DEHYDROGENASE; ADENOSINE TRIPHOSPHATASE (CALCIUM); ADENOSINE TRIPHOSPHATASE CALCIUM TRANSPORTING, CARDIAC MUSCLE SLOW TWITCH 2; CARNITINE PALMITOYLTRANSFERASE; CASPASE 3; CERAMIDE; CITRATE SYNTHASE; CYCLOPHILIN; GLUCOSE TRANSPORTER 4; MESENCEPHALIC ASTROCYTE DERIVED NEUROTROPHIC FACTOR; MITOCHONDRIAL ENZYME; MYOSIN HEAVY CHAIN ALPHA; MYOSIN HEAVY CHAIN BETA; MYOSIN VIIA; NATRIURETIC PEPTIDE RECEPTOR B; PEPTIDYLPROLYL ISOMERASE; PEROXISOME PROLIFERATOR ACTIVATED RECEPTOR GAMMA COACTIVATOR 1ALPHA; PEROXISOME PROLIFERATOR ACTIVATED RECEPTOR GAMMA COACTIVATOR 1BETA; PHOSPHOPROTEIN PHOSPHATASE 2A; PROTEIN KINASE B; UNCLASSIFIED DRUG; PHOSPHOPROTEIN PHOSPHATASE 2; PPARGC1A PROTEIN, MOUSE; SLC2A4 PROTEIN, MOUSE;

ADAPTATION; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; AORTIC CONSTRICTION; APOPTOSIS; ARTICLE; CELLULAR STRESS RESPONSE; CONTROLLED STUDY; ENDURANCE TRAINING; ENZYME ACTIVITY; GLUCOSE METABOLISM; HEART FAILURE; HEART HEMODYNAMICS; HEART LEFT VENTRICLE OVERLOAD; HEART MUSCLE CONTRACTILITY; HEART MUSCLE FIBROSIS; HEART VENTRICLE HYPERTROPHY; HEMODYNAMIC STRESS; MITOCHONDRIAL RESPIRATION; MOUSE; NONHUMAN; OXIDATIVE STRESS; PHYSIOLOGICAL STRESS; PRIORITY JOURNAL; PROTEIN DEPHOSPHORYLATION; PROTEIN EXPRESSION; SWIMMING; ANIMAL; AORTA; CARDIAC MUSCLE; CARDIOMEGALY; DEFICIENCY; DISEASE MODEL; EXERCISE; EXERCISE INDUCED CARDIOMEGALY; GENETIC PREDISPOSITION; GENETICS; HEART CONTRACTION; HEART LEFT VENTRICLE FUNCTION; HEART VENTRICLE REMODELING; HEMODYNAMICS; KNOCKOUT MOUSE; LIGATION; METABOLISM; PATHOLOGY; PATHOPHYSIOLOGY; PHENOTYPE; SURGERY;

3-HYDROXYACYL COA DEHYDROGENASES; ADAPTATION, PHYSIOLOGICAL; ANIMALS; AORTA; CARDIOMEGALY; CARDIOMEGALY, EXERCISE-INDUCED; CARNITINE O-PALMITOYLTRANSFERASE; CONSTRICTION; DISEASE MODELS, ANIMAL; GENETIC PREDISPOSITION TO DISEASE; GLUCOSE TRANSPORTER TYPE 4; HEMODYNAMICS; MICE, KNOCKOUT; MYOCARDIAL CONTRACTION; MYOCARDIUM; PEROXISOME PROLIFERATOR-ACTIVATED RECEPTOR GAMMA COACTIVATOR 1-ALPHA; PHENOTYPE; PHYSICAL EXERTION; PROTEIN PHOSPHATASE 2; PROTO-ONCOGENE PROTEINS C-AKT; VENTRICULAR FUNCTION, LEFT; VENTRICULAR REMODELING;

EID: 85037053775     PISSN: 03636135     EISSN: 15221539     Source Type: Journal    
DOI: 10.1152/ajpheart.00101.2017     Document Type: Article

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