Excessive thyroxine enhances susceptibility to apoptosis and decreases contractility of cardiomyocytes

Molecular and Cellular Endocrinology

Volumn 320, Issue 1-2, 2010, Pages 67-75

  Wang, Yun Ying ^a   Jiao, Bo ^a   Guo, Wang Gang ^a   Che, Hong Lei ^a   Yu, Zhi Bin ^a  

^a FOURTH MILITARY MEDICAL UNIVERSITY   (China)

Author keywords

Apoptosis; Cardiac hypertrophy; Contractility; Heart failure; Hyperthyroid

Indexed keywords

ANGIOTENSIN II; DNA; LEVOTHYROXINE; LIOTHYRONINE; THYROXINE;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; APOPTOSIS; ARTICLE; CONTROLLED STUDY; HEART CELL CULTURE; HEART CONTRACTION; HEART FAILURE; HEART MUSCLE CELL; HEART MUSCLE CONTRACTILITY; HEART STROKE VOLUME; HEART VENTRICLE HYPERTROPHY; HYPERTHYROIDISM; HYPERTROPHY; MALE; NONHUMAN; PRIORITY JOURNAL; RAT;

ANIMALS; APOPTOSIS; CELL SEPARATION; CELL SIZE; CELLS, CULTURED; DNA FRAGMENTATION; HEART RATE; HYPERTHYROIDISM; IN SITU NICK-END LABELING; MALE; MYOCARDIAL CONTRACTION; MYOCARDIUM; MYOCYTES, CARDIAC; NECROSIS; ORGAN SIZE; RATS; RATS, SPRAGUE-DAWLEY; STROKE VOLUME; SURFACE PROPERTIES; THYROXINE;

EID: 77949566585     PISSN: 03037207     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.mce.2010.01.031     Document Type: Article

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