ArticleCardiovascular research2013
c-Jun N-terminal kinase activation contributes to reduced connexin43 and development of atrial arrhythmias.
Article in Cardiovascular research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 3 of them syntheses that pooled it.
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Who cites it
48 citing papers in PubMed, 3 syntheses or guidelines pooled it, 71 citations in OpenAlex.
- 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines.Journal of the American College of Cardiology · 2024Guideline
- Guideline
- Association BetweenFrontiers in cardiovascular medicine · 2020Pooled it
- JNK2 Is a Stress Integrator Driving Atrial Fibrillation Pathogenesis in Aging via Gut-Heart Crosstalk.Circulation · 2026Article
- Mechanisms of Atrial Fibrillation in Heart Failure: Uncovering Therapeutic Targets in the Atrial Substrate.Current heart failure reports · 2026Review
- Deceiving the gatekeepers: virus modulation of gap junctions.Microbiology and molecular biology reviews : MMBR · 2025Review
- Stress-Induced calcium mishandling in cardiac (Patho)physiology.Cellular and molecular life sciences : CMLS · 2025Review
- The Interplay Between Pulmonary Hypertension and Atrial Fibrillation: A Comprehensive Overview.Cells · 2025Review
- Alda-1 attenuation of binge alcohol-caused atrial arrhythmias through a novel mechanism of suppressed c-Jun N-terminal Kinase-2 activity.Journal of molecular and cellular cardiology · 2024Article
- Noise Exposure in the Workplace, Genetic Susceptibility, and Incidence of Atrial Fibrillation: A Prospective Cohort Study.Journal of the American Heart Association · 2024Article
- The role of cellular senescence in profibrillatory atrial remodelling associated with cardiac pathology.Cardiovascular research · 2024Article
- Differentially expressed transcripts study during pregnancy and postpartum anestrus of yak (Animal biotechnology · 2023Article
- p38γ/δ activation alters cardiac electrical activity and predisposes to ventricular arrhythmia.Nature cardiovascular research · 2023Article
- Long-Term Alcohol-Activated c-Jun N-terminal Kinase Isoform 2 Preserves Cardiac Function but Drives CaCells · 2023Article
- Advances in basic and translational research in atrial fibrillation.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Review
- Mitochondrial Connexins and Mitochondrial Contact Sites with Gap Junction Structure.International journal of molecular sciences · 2023Review
- Cannabinoid receptor agonist attenuates angiotensin II-induced enlargement and mitochondrial dysfunction in rat atrial cardiomyocytes.Frontiers in pharmacology · 2023Article
- Mechanisms of Quercetin against atrial fibrillation explored by network pharmacology combined with molecular docking and experimental validation.Scientific reports · 2022Article
- Review
- S-nitrosylation of c-Jun N-terminal kinase mediates pressure overload-induced cardiac dysfunction and fibrosis.Acta pharmacologica Sinica · 2022Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
aimsc-Jun N-terminal kinase (JNK) activation is implicated in cardiovascular diseases and ageing, which are linked to enhanced propensity to atrial fibrillation (AF). However, the contribution of JNK to AF remains unknown. Thus, we assessed the role of JNK in remodelling of gap junction connexin43 (Cx43) and development of AF. METHODS AND
resultsAF induction, optical mapping, and biochemical assays were performed in young and aged New Zealand white rabbit left atria (LA) and cultured HL-1 atrial cells. In aged rabbit LA, pacing-induced atrial arrhythmias were dramatically increased and conduction velocity (CV) was significantly slower compared with young controls. Aged rabbit LA contained 120% more activated JNK and 54% less Cx43 than young LA. Young rabbits treated with JNK activator anisomycin also exhibited increased pacing-induced atrial arrhythmias and reduced Cx43 (by 34%), similar to that found in aged LA. In HL-1 cell cultures, anisomycin treatment for 16 h led to 42% reduction in Cx43, 24% reduction in CV, and an increased incidence of irregular rapid spontaneous activities. These effects were prevented by a specific JNK inhibitor, SP600125. Moreover, a 63% reduction in Cx43 after anisomycin treatment for 24 h led to further slowed CV (by 41%) along with dramatically increased irregular rapid spontaneous activity and highly discontinuous conduction. These JNK-induced functional abnormalities were completely reversed by overexpressed exogenous wild-type Cx43, but not by inactive Cx43.
conclusionJNK activation contributes to Cx43 reductions that promote development of AF. Modulation of JNK may be a potential novel therapeutic approach to prevent and treat AF.
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Registered trials
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