Hou, Xiaoyang <br/><br/>
PPAR-γ activation by rosiglitazone suppresses angiotensin II-mediated proliferation and phenotypictransition in cardiac fibroblasts via inhibition of activation of activator protein 1.  [electronic resource] 

 -  European journal of pharmacology  Sep 2013 
 - 196-203 p.  digital 
<br/><br/> Publication Type: Journal Article; Research Support, Non-U.S. Gov't 
<br/><br/><label>ISSN: </label>1879-0712 
<br/><br/><label>Standard No.: </label>10.1016/j.ejphar.2013.05.021  doi 
<br/><br/><label>Subjects--Topical Terms: </label><br/>Angiotensin II--pharmacology<br/>Animals<br/>Cell Differentiation--drug effects<br/>Cell Proliferation--drug effects<br/>Cell Survival--drug effects<br/>Collagen Type I--genetics<br/>Collagen Type III--genetics<br/>Cyclin D1--genetics<br/>Fibroblasts--cytology<br/>JNK Mitogen-Activated Protein Kinases--chemistry<br/>Myocardium--cytology<br/>Myofibroblasts--cytology<br/>PPAR gamma--metabolism<br/>Phenotype<br/>Protein Multimerization--drug effects<br/>Protein Structure, Quaternary<br/>Proto-Oncogene Proteins c-fos--chemistry<br/>RNA, Messenger--genetics<br/>Rats<br/>Rats, Wistar<br/>Rosiglitazone<br/>Thiazolidinediones--pharmacology<br/>Transcription Factor AP-1--metabolism<br/>Transforming Growth Factor beta1--genetics