ReviewJournal of molecular and cellular cardiology2008
Is there a role for remodeled connexins in AF? No simple answers.
Review in Journal of molecular and cellular cardiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 60 citations in OpenAlex.
- EXPRESSION OF CONNEXIN-40 AND INTERLEUKIN 6 GENES IN PATIENTS WITH ATRIAL FIBRILLATION.Acta clinica Croatica · 2025Article
- Research progress of connexin 43 in cardiovascular diseases.Frontiers in cardiovascular medicine · 2025Review
- Synergistic Effects of Weight Loss and Catheter Ablation: Can microRNAs Serve as Predictive Biomarkers for the Prevention of Atrial Fibrillation Recurrence?International journal of molecular sciences · 2024Review
- Review
- Connexin Lateralization Contributes to Male Susceptibility to Atrial Fibrillation.International journal of molecular sciences · 2022Article
- Review
- Serine-threonine protein phosphatase regulation of Cx43 dephosphorylation in arrhythmogenic disorders.Cellular signalling · 2021Review
- Galectin-3 in Atrial Fibrillation: Mechanisms and Therapeutic Implications.International journal of molecular sciences · 2018Review
- Chronic Kidney Disease Increases Atrial Fibrillation Inducibility: Involvement of Inflammation, Atrial Fibrosis, and Connexins.Frontiers in physiology · 2018Article
- The stress kinase JNK regulates gap junction Cx43 gene expression and promotes atrial fibrillation in the aged heart.Journal of molecular and cellular cardiology · 2018Article
- Connexins in Cardiovascular and Neurovascular Health and Disease: Pharmacological Implications.Pharmacological reviews · 2017Review
- Cardiac Cx43, Cx40 and Cx45 co-assembling: involvement of connexins epitopes in formation of hemichannels and Gap junction channels.BMC cell biology · 2017Review
- An atrial-fibrillation-linked connexin40 mutant is retained in the endoplasmic reticulum and impairs the function of atrial gap-junction channels.Disease models & mechanisms · 2014Article
- Targeting inflammation and oxidative stress in atrial fibrillation: role of 3-hydroxy-3-methylglutaryl-coenzyme a reductase inhibition with statins.Antioxidants & redox signaling · 2014Review
- c-Jun N-terminal kinase activation contributes to reduced connexin43 and development of atrial arrhythmias.Cardiovascular research · 2013Article
- Effect of renal sympathetic denervation on atrial substrate remodeling in ambulatory canines with prolonged atrial pacing.PloS one · 2013Article
- Triggers and anatomical substrates in the genesis and perpetuation of atrial fibrillation.Current cardiology reviews · 2012Review
- The molecular mechanisms of gap junction remodeling.Heart rhythm · 2012Review
- Effects of metoprolol therapy on cardiac gap junction remodelling and conduction in human chronic atrial fibrillation.British journal of pharmacology · 2011Article
- Inflammatory responses in the atria: should they stay or should they go?Heart rhythm · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Gap junctions provide direct cytoplasmic continuity between cells forming a low resistivity barrier to electrical propagation. As such, aberrant regulation of these low resistive conduits has been blamed for electrical conduction disorders in diseased myocardium. While there is a plethora of evidence that abnormalities in gap junctional communication underlie many forms of ventricular arrhythmias, the role of gap junctions in atrial conduction disorders has been less well studied. The atria are the most heterogeneous cardiac structures in terms of the gap junction proteins, connexins (Cx), which are present. Cx40 is the primary, or most abundant, gap junction protein in atria although Cx43 is also abundantly expressed. Cx45 is also expressed in atria, although at low levels. This heterogeneity in connexins leads to a complexity that makes understanding the role of cell coupling in conduction disorders and arrhythmogenesis difficult. In this review we focus on what is known about atrial connexins and their role in atrial fibrillation but also on the challenges presented in understanding the complex interplay between the individual connexin isoforms.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.