Expression of G qα and PLC-β in Scar and Border Tissue in Heart Failure Due to Myocardial Infarction
Author(s) -
Haisong Ju,
Shufang Zhao,
Paramjit S. Tappia,
Vincenzo Panagia,
Ian Dixon
Publication year - 1998
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/01.cir.97.9.892
Subject(s) - heart failure , medicine , gq alpha subunit , myocardial infarction , ventricle , cardiology , downregulation and upregulation , endocrinology , myocyte , fibrosis , ventricular remodeling , endothelin receptor , angiotensin ii , receptor , g protein , biology , biochemistry , gene
Large transmural myocardial infarction (MI) leads to maladaptive cardiac remodeling and places patients at increased risk of congestive heart failure. Angiotensin II, endothelin, and alpha1-adrenergic receptor agonists are implicated in the development of cardiac hypertrophy, interstitial fibrosis, and heart failure after MI. Because these agonists are coupled to and activate Gq alpha protein in the heart, the aim of the present study was to investigate Gq alpha expression and function in cardiac remodeling and heart failure after MI.
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