ArticleInternational journal of cardiology2013
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.
Article in International journal of cardiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 57 citations in OpenAlex.
- Gut microbial trimethylamine N-oxide generation promotes risk of atrial fibrillation via muscarinic receptor-mediated autonomic dysfunction.The Journal of clinical investigation · 2026Article
- Exercise preconditioning reduces the electrostimulation-induced incidence of arrhythmias in exhausted rats by regulating the CaMKⅡ-RyR2 signaling pathway.Journal of cardiothoracic surgery · 2026Article
- A modification of retrograde Langendorff-perfusion to increase the yield of CaFrontiers in pharmacology · 2026Article
- Thyrotropin Directly Affects Cardiac Electrophysiology and Is Associated With AF Prevalence.Circulation. Arrhythmia and electrophysiology · 2025Article
- Atrial cardiomyocyte-restricted cleavage of gasdermin D promotes atrial arrhythmogenesis.European heart journal · 2025Article
- Cathepsin Levels and Atrial Fibrillation Risk: Insights From Bidirectional and Multivariable Mendelian Randomization Analyses.International journal of genomics · 2025Article
- Atrial Proteomic Profiling Reveals a Switch Towards Profibrotic Gene Expression Program in CREM-IbΔC-X Mice with Persistent Atrial Fibrillation.bioRxiv : the preprint server for biology · 2024Article
- Mouse models of spontaneous atrial fibrillation.Mammalian genome : official journal of the International Mammalian Genome Society · 2023Review
- PI3K(p110α) as a determinant and gene therapy for atrial enlargement in atrial fibrillation.Molecular and cellular biochemistry · 2023Review
- Guidelines for assessment of cardiac electrophysiology and arrhythmias in small animals.American journal of physiology. Heart and circulatory physiology · 2022Review
- Genetic inhibition of nuclear factor of activated T-cell c2 prevents atrial fibrillation in CREM transgenic mice.Cardiovascular research · 2022Article
- Transcriptional factors in calcium mishandling and atrial fibrillation development.Pflugers Archiv : European journal of physiology · 2021Review
- The crosstalk between cardiomyocyte calcium and inflammasome signaling pathways in atrial fibrillation.Pflugers Archiv : European journal of physiology · 2021Review
- Inward Rectifier KJournal of the American Heart Association · 2020Article
- Inflammasomes and Proteostasis Novel Molecular Mechanisms Associated With Atrial Fibrillation.Circulation research · 2020Review
- The Genetic Puzzle of Familial Atrial Fibrillation.Frontiers in cardiovascular medicine · 2020Review
- HDAC (Histone Deacetylase) Inhibitor Valproic Acid Attenuates Atrial Remodeling and Delays the Onset of Atrial Fibrillation in Mice.Circulation. Arrhythmia and electrophysiology · 2019Article
- Genetic Regulation of Liver Metabolites and Transcripts Linking to Biochemical-Clinical Parameters.Frontiers in genetics · 2019Article
- Article
- Atrial thrombogenesis in atrial fibrillation : Results from atrial fibrillation models and AF-patients.Herzschrittmachertherapie & Elektrophysiologie · 2018Review
Corrections and comments
- Erratum issued
Authors and funding
24 authors at 6 institutions in 4 countries.
Funding
Abstract
BACKGROUND AND
methodsAtrial 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-IbΔC-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.
resultsOverexpression of CREM-IbΔC-X in young TG mice (<8weeks) led to atrial dilatation combined with distension of myocardium, elongated myocytes, little fibrosis, down-regulation of connexin 40, loss of excitability with a number of depolarized myocytes, atrial ectopies and inducibility of AF. These abnormalities continuously progressed with age resulting in interatrial conduction block, increased atrial conduction heterogeneity, leaky sarcoplasmic reticulum calcium stores and the spontaneous occurrence of paroxysmal and later persistent AF. This distinct atrial remodelling was associated with a pattern of non-regulated and up-regulated marker genes of myocardial hypertrophy and fibrosis.
conclusionsExpression of CREM-IbΔC-X in TG hearts evokes abnormal growth and development of the atria preceding conduction abnormalities and altered calcium homeostasis and the development of spontaneous and persistent AF. We conclude that transcription factor CREM is an important regulator of atrial growth implicated in the development of an arrhythmogenic substrate in TG mice.
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