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Cardiomyocyte cyclooxygenase-2 influences cardiac rhythm and function.

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.

Pubmed ID: 19376970


  • Wang D
  • Patel VV
  • Ricciotti E
  • Zhou R
  • Levin MD
  • Gao E
  • Yu Z
  • Ferrari VA
  • Lu MM
  • Xu J
  • Zhang H
  • Hui Y
  • Cheng Y
  • Petrenko N
  • Yu Y
  • FitzGerald GA


Proceedings of the National Academy of Sciences of the United States of America

Publication Data

May 5, 2009

Associated Grants

  • Agency: NHLBI NIH HHS, Id: HL 622050
  • Agency: NHLBI NIH HHS, Id: K08 HL074108
  • Agency: NHLBI NIH HHS, Id: KO8 HL074108
  • Agency: NHLBI NIH HHS, Id: R01 HL081185
  • Agency: NHLBI NIH HHS, Id: R01 HL081185-03
  • Agency: NCRR NIH HHS, Id: RR 023567

Mesh Terms

  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal
  • Cyclooxygenase 2
  • Gene Deletion
  • Heart Rate
  • Hypertrophy
  • Mice
  • Mice, Knockout
  • Myocytes, Cardiac