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 Moubarak; Xander H. T. Wehrens; Wilhelm Schmitz; Stephane Hatem; Frank Ulrich Mueller

doi:10.1016/j.ijcard.2011.10.057

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 journal › Article › Academic › peer-review

Abstract

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 language	English
Pages (from-to)	366-374
Journal	International Journal of Cardiology
Volume	166
Issue number	2
DOIs	https://doi.org/10.1016/j.ijcard.2011.10.057
Publication status	Published - 20 Jun 2013

Keywords

Atrial fibrillation
Transgenic mice
Substrate remodelling
cAMP-dependent gene regulation

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10.1016/j.ijcard.2011.10.057

Cite this

Kirchhof, P., Marijon, E., Fabritz, L., Li, N., Wang, W., Wang, T., Schulte, K., Hanstein, J., Schulte, J. S., Vogel, M., Mougenot, N., Laakmann, S., Fortmueller, L., Eckstein, J., Verheule, S., Kaese, S., Staab, A., Grote-Wessels, S., Schotten, U., ... Mueller, F. U. (2013). 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. International Journal of Cardiology, 166(2), 366-374. https://doi.org/10.1016/j.ijcard.2011.10.057

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title = "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",

abstract = "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 (",

keywords = "Atrial fibrillation, Transgenic mice, Substrate remodelling, cAMP-dependent gene regulation",

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

year = "2013",

month = jun,

day = "20",

doi = "10.1016/j.ijcard.2011.10.057",

language = "English",

volume = "166",

pages = "366--374",

journal = "International Journal of Cardiology",

issn = "0167-5273",

publisher = "Elsevier Ireland Ltd",

number = "2",

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Kirchhof, P, Marijon, E, Fabritz, L, Li, N, Wang, W, Wang, T, Schulte, K, Hanstein, J, Schulte, JS, Vogel, M, Mougenot, N, Laakmann, S, Fortmueller, L, Eckstein, J, Verheule, S, Kaese, S, Staab, A, Grote-Wessels, S, Schotten, U, Moubarak, G, Wehrens, XHT, Schmitz, W, Hatem, S & Mueller, FU 2013, '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', International Journal of Cardiology, vol. 166, no. 2, pp. 366-374. https://doi.org/10.1016/j.ijcard.2011.10.057

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. / Kirchhof, Paulus; Marijon, Eloi; Fabritz, Larissa et al.
In: International Journal of Cardiology, Vol. 166, No. 2, 20.06.2013, p. 366-374.

Research output: Contribution to journal › Article › Academic › peer-review

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 -