Anti-apoptotic effect of heat shock protein 90 on hypoxia-mediated cardiomyocyte damage is mediated via the phosphatidylinositol 3-kinase/akt pathway

Clinical and Experimental Pharmacology and Physiology

Volumn 36, Issue 9, 2009, Pages 899-903

  Wang, Wei ^a   Peng, Yizhi ^a   Wang, Yuanyuan ^a   Zhao, Xiaohui ^a   Yuan, Zhiqiang ^a  

^a THIRD MILITARY MEDICAL UNIVERSITY   (China)

Author keywords

Apoptosis; Cardiomyocyte; Heart failure; Heat shock protein 90; Hypoxia; Phosphatidylinositol 3 kinase Akt signalling pathway; Serine threonine protein kinase Akt

Indexed keywords

CASPASE 3; CYTOCHROME C; DNA NUCLEOTIDYLEXOTRANSFERASE; GELDANAMYCIN; HEAT SHOCK PROTEIN 90; LACTATE DEHYDROGENASE; PHOSPHATIDYLINOSITOL 3 KINASE; PROTEIN BAD; PROTEIN KINASE B;

ANIMAL CELL; ANIMAL CELL CULTURE; APOPTOSIS; ARTICLE; CONTROLLED STUDY; ENZYME ACTIVITY; ENZYME RELEASE; HEART MUSCLE INJURY; HYPOXIA; NEWBORN; NONHUMAN; PROTEIN EXPRESSION; RAT; WESTERN BLOTTING;

ANIMALS; ANIMALS, NEWBORN; APOPTOSIS; BCL-ASSOCIATED DEATH PROTEIN; BENZOQUINONES; BLOTTING, WESTERN; CASPASE 3; CELL HYPOXIA; CELLS, CULTURED; CYTOCHROMES C; CYTOPROTECTION; HSP90 HEAT-SHOCK PROTEINS; IN SITU NICK-END LABELING; L-LACTATE DEHYDROGENASE; LACTAMS, MACROCYCLIC; MYOCYTES, CARDIAC; PHOSPHATIDYLINOSITOL 3-KINASE; PHOSPHORYLATION; PROTO-ONCOGENE PROTEINS C-AKT; RATS; RATS, WISTAR; SIGNAL TRANSDUCTION; TIME FACTORS;

EID: 69949087513     PISSN: 03051870     EISSN: 14401681     Source Type: Journal    
DOI: 10.1111/j.1440-1681.2009.05167.x     Document Type: Article

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