| Literature DB >> 19376970 |
Dairong Wang1, Vickas V Patel, Emanuela Ricciotti, Rong Zhou, Mark D Levin, Ehre Gao, Zhou Yu, Victor A Ferrari, Min Min Lu, Junwang Xu, Hualei Zhang, Yiqun Hui, Yan Cheng, Nataliya Petrenko, Ying Yu, Garret A FitzGerald.
Abstract
Nonsteroidal anti-inflammatory drugs selective for inhibition of COX-2 increase heart failure and elevate blood pressure. The COX-2 gene was floxed and crossed into merCremer mice under the alpha-myosin heavy-chain promoter. Tamoxifen induced selective deletion of COX-2 in cardiomyocytes depressed cardiac output, and resulted in weight loss, diminished exercise tolerance, and enhanced susceptibility to induced arrhythmogenesis. The cardiac dysfunction subsequent to pressure overload recovered progressively in the knockouts coincident with increasing cardiomyocyte hypertrophy and interstitial and perivascular fibrosis. Inhibition of COX-2 in cardiomyocytes may contribute to heart failure in patients receiving nonsteroidal anti-inflammatory drugs specific for inhibition of COX-2.Entities:
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Year: 2009 PMID： 19376970 PMCID： PMC2670242 DOI： 10.1073/pnas.0805806106
Source DB: PubMed Journal: Proc Natl Acad Sci U S A ISSN： 0027-8424 Impact factor: 11.205