TY - JOUR
T1 - 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
AU - Kirchhof, Paulus
AU - Marijon, Eloi
AU - Fabritz, Larissa
AU - Li, Na
AU - Wang, Wei
AU - Wang, Tiannan
AU - Schulte, Kirsten
AU - Hanstein, Juliane
AU - Schulte, Jan S.
AU - Vogel, Mathis
AU - Mougenot, Nathalie
AU - Laakmann, Sandra
AU - Fortmueller, Lisa
AU - Eckstein, Jens
AU - Verheule, Sander
AU - Kaese, Sven
AU - Staab, Ariane
AU - Grote-Wessels, Stephanie
AU - Schotten, Ulrich
AU - Moubarak, Ghassan
AU - Wehrens, Xander H. T.
AU - Schmitz, Wilhelm
AU - Hatem, Stephane
AU - Mueller, Frank Ulrich
PY - 2013/6/20
Y1 - 2013/6/20
N2 - 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 (
AB - 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 (
KW - Atrial fibrillation
KW - Transgenic mice
KW - Substrate remodelling
KW - cAMP-dependent gene regulation
U2 - 10.1016/j.ijcard.2011.10.057
DO - 10.1016/j.ijcard.2011.10.057
M3 - Article
C2 - 22093963
SN - 0167-5273
VL - 166
SP - 366
EP - 374
JO - International Journal of Cardiology
JF - International Journal of Cardiology
IS - 2
ER -