Cisplatin compromises myocardial contractile function and mitochondrial ultrastructure: Role of endoplasmic reticulum stress

Clinical and Experimental Pharmacology and Physiology

Volumn 37, Issue 4, 2010, Pages 460-465

  Ma, Heng ^a,c   Jones, Kyla R ^a   Guo, Rui ^a   Xu, Peisheng ^a   Shen, Youqing ^b   Ren, Jun ^a,c  

^a Center for Cardiovascular Research and Alternative Medicine   (United States)

^b UNIVERSITY OF WYOMING   (United States)

^c FOURTH MILITARY MEDICAL UNIVERSITY   (China)

Author keywords

Cardiotoxicity; Cisplatin; Endoplasmic reticulum stress; Mitochondrial abnormalities

Indexed keywords

CASPASE 3; CISPLATIN; GLUCOSE REGULATED PROTEIN 78; INITIATION FACTOR 2ALPHA;

ANIMAL CELL; ANIMAL EXPERIMENT; APOPTOSIS; ARTICLE; CARDIOTOXICITY; CELL ULTRASTRUCTURE; CONTROLLED STUDY; ENDOPLASMIC RETICULUM STRESS; ENZYME ACTIVITY; HEART CONTRACTION; HEART DEPOLARIZATION; HEART DISEASE; HEART FUNCTION; HEART LEFT VENTRICLE DP-DT; HEART LEFT VENTRICLE PRESSURE; HEART MITOCHONDRION; MITOCHONDRIAL MEMBRANE POTENTIAL; MOUSE; NICK END LABELING; NONHUMAN; PROTEIN EXPRESSION; PROTEIN PHOSPHORYLATION; TRANSMISSION ELECTRON MICROSCOPY; UPREGULATION;

ANIMALS; ANTINEOPLASTIC AGENTS; APOPTOSIS; CARDIOTOXINS; CASPASE 3; CELL SHAPE; CELLS, CULTURED; CISPLATIN; DEPRESSION, CHEMICAL; ENDOPLASMIC RETICULUM; HEART; HEMODYNAMICS; MALE; MEMBRANE POTENTIAL, MITOCHONDRIAL; MICE; MICE, INBRED C57BL; MITOCHONDRIA, HEART; MYOCARDIAL CONTRACTION; MYOCARDIUM; MYOCYTES, CARDIAC; ORGAN SIZE; STRESS, PHYSIOLOGICAL;

EID: 77949911469     PISSN: 03051870     EISSN: 14401681     Source Type: Journal    
DOI: 10.1111/j.1440-1681.2009.05323.x     Document Type: Article

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