Overexpression of cAMP-response element modulator causes abnormal growth and development of the atrial myocardium resulting in a substrate for sustained atrial fibrillation in mice

Paulus Kirchhof, Eloi Marijon, Larissa Fabritz, Na Li, Wei Wang, Tiannan Wang, Kirsten Schulte, Juliane Hanstein, Jan S. Schulte, Mathis Vogel, Nathalie Mougenot, Sandra Laakmann, Lisa Fortmueller, Jens Eckstein, Sander Verheule, Sven Kaese, Ariane Staab, Stephanie Grote-Wessels, Ulrich Schotten, Ghassan MoubarakXander H. T. Wehrens, Wilhelm Schmitz, Stephane Hatem, Frank Ulrich Mueller*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

39 Citations (Web of Science)


Background and methods: Atrial fibrillation (AF) is the most common cardiac arrhythmia in clinical practice. The substrate of AF is composed of a complex interplay between structural and functional changes of the atrial myocardium often preceding the occurrence of persistent AF. However, there are only few animal models reproducing the slow progression of the AF substrate to the spontaneous occurrence of the arrhythmia. Transgenic mice (TG) with cardiomyocyte-directed expression of CREM-Ib Delta C-X, an isoform of transcription factor CREM, develop atrial dilatation and spontaneous-onset AF. Here we tested the hypothesis that TG mice develop an arrhythmogenic substrate preceding AF using physiological and biochemical techniques. Results: Overexpression of CREM-Ib Delta C-X in young TG mice (
Original languageEnglish
Pages (from-to)366-374
JournalInternational Journal of Cardiology
Issue number2
Publication statusPublished - 20 Jun 2013


  • Atrial fibrillation
  • Transgenic mice
  • Substrate remodelling
  • cAMP-dependent gene regulation

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