TGF-β improves myocardial function and prevents apoptosis induced by anoxia–reoxygenation, through the reduction of endoplasmic reticulum stress

Canadian Journal of Physiology and Pharmacology

Volumn 94, Issue 1, 2015, Pages 9-17

  Wang, Yufeng ^a   Zong, Ligeng ^b   Wang, Xiaolei ^c  

^a Wendeng Central Hospital   (China)

^b BINZHOU PEOPLE S HOSPITAL   (China)

^c Traditional Chinese Medicine Hospital of Yantai   (China)

Author keywords

Anoxia reoxygenation; Apoptosis; Endoplasmic reticulum stress; Ischemia reperfusion injury; TGF

Indexed keywords

CASPASE 12; CASPASE 3; GLUCOSE REGULATED PROTEIN 78; GROWTH ARREST AND DNA DAMAGE INDUCIBLE PROTEIN 153; MESSENGER RNA; PROTEIN BAX; PROTEIN BCL 2; REACTIVE OXYGEN METABOLITE; RECOMBINANT TRANSFORMING GROWTH FACTOR BETA; STRESS ACTIVATED PROTEIN KINASE; CASP3 PROTEIN, RAT; CASPASE INHIBITOR; RECOMBINANT PROTEIN; TRANSFORMING GROWTH FACTOR BETA;

ADULT; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; APOPTOSIS; ARTICLE; CELL HYPOXIA; CELL MEMBRANE DEPOLARIZATION; CELL VIABILITY; CONCENTRATION RESPONSE; CONTROLLED STUDY; DOSE RESPONSE; ENDOPLASMIC RETICULUM STRESS; ENZYME ACTIVITY; HEART FUNCTION; HEART MUSCLE CELL; HEART MUSCLE CONTRACTILITY; HEART MUSCLE ISCHEMIA; HEART PROTECTION; MALE; MITOCHONDRIAL MEMBRANE POTENTIAL; NONHUMAN; PRIORITY JOURNAL; PROTEIN EXPRESSION; RAT; REOXYGENATION; REPERFUSION INJURY; TUNEL ASSAY; ANIMAL; CARDIAC MUSCLE CELL; CELL LINE; CYTOLOGY; DRUG EFFECTS; HEART; METABOLISM; MYOCARDIAL REPERFUSION INJURY; PATHOLOGY; PATHOPHYSIOLOGY; PHYSIOLOGY;

ANIMALS; APOPTOSIS; CASPASE 3; CASPASE INHIBITORS; CELL LINE; ENDOPLASMIC RETICULUM STRESS; HEART; MEMBRANE POTENTIAL, MITOCHONDRIAL; MYOCARDIAL REPERFUSION INJURY; MYOCYTES, CARDIAC; RATS; REACTIVE OXYGEN SPECIES; RECOMBINANT PROTEINS; TRANSFORMING GROWTH FACTOR BETA;

EID: 84953398172     PISSN: 00084212     EISSN: 12057541     Source Type: Journal    
DOI: 10.1139/cjpp-2014-0466     Document Type: Article

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