ArticleThe Journal of clinical investigation2024
Modulation of NOX2 causes obesity-mediated atrial fibrillation.
Article in The Journal of clinical investigation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Freely available genomic datasets for atrial fibrillation research: current resources and analytical pipeline.Frontiers in genetics · 2026Pooled it
- Role of NADPH oxidase 2-derived reactive oxygen species in cardiac electrophysiological disorders.Channels (Austin, Tex.) · 2026Review
- Association of the chemerin-CMKLR1 with atrial potassium current dysregulation and atrial fibrillation in obese mice.Channels (Austin, Tex.) · 2026Article
- The clinical pathophysiology of atrial fibrillation: outstanding questions from bedside to bench and back.Physiological reviews · 2026Review
- Chrysin Attenuates Dry Eye Progression by Suppressing NOX2-Dependent Ferroptosis and STING/NLRP3-Mediated Inflammatory Responses.Investigative ophthalmology & visual science · 2026Article
- Gene-gene interactions between a LMNA variant and common polymorphisms drive early-onset atrial fibrillation.Nature communications · 2026Article
- A New Paradigm for Atrial Fibrillation Ablation in Obesity Focusing on Substrate Remodeling and Patient-Centered Outcomes.Reviews in cardiovascular medicine · 2026Review
- Atrial fibrillation and metabolic syndrome: an updated review of mechanisms, risk factors, and therapeutic strategies.Frontiers in cardiovascular medicine · 2026Review
- Cardiometabolic disease and cardio-oncology: Insights from iPSC models and tissue engineering.Cell reports. Medicine · 2025Review
- Association Between Blood Free Fatty Acid Concentrations in Midlife and Cerebral Small Vessel Disease.Antioxidants (Basel, Switzerland) · 2025Article
- Molecular Insights into Oxidative-Stress-Mediated Cardiomyopathy and Potential Therapeutic Strategies.Biomolecules · 2025Review
- p21-Activated Kinase 1 (Pak1) as an Element in Functional and Dysfunctional Interplay Among the Myocardium, Adipose Tissue, and Pancreatic Beta Cells.Comprehensive Physiology · 2025Review
- Identification of Putative Serum Autoantibodies Associated with Post-Acute Sequelae of COVID-19 via Comprehensive Protein Array Analysis.International journal of molecular sciences · 2025Article
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
Obesity is linked to an increased risk of atrial fibrillation (AF) via increased oxidative stress. While NADPH oxidase 2 (NOX2), a major source of oxidative stress and reactive oxygen species (ROS) in the heart, predisposes to AF, the underlying mechanisms remain unclear. Here, we studied NOX2-mediated ROS production in obesity-mediated AF using Nox2-knockout mice and mature human induced pluripotent stem cell-derived atrial cardiomyocytes (hiPSC-aCMs). Diet-induced obesity (DIO) mice and hiPSC-aCMs treated with palmitic acid (PA) were infused with a NOX blocker (apocynin) and a NOX2-specific inhibitor, respectively. We showed that NOX2 inhibition normalized atrial action potential duration and abrogated obesity-mediated ion channel remodeling with reduced AF burden. Unbiased transcriptomics analysis revealed that NOX2 mediates atrial remodeling in obesity-mediated AF in DIO mice, PA-treated hiPSC-aCMs, and human atrial tissue from obese individuals by upregulation of paired-like homeodomain transcription factor 2 (PITX2). Furthermore, hiPSC-aCMs treated with hydrogen peroxide, a NOX2 surrogate, displayed increased PITX2 expression, establishing a mechanistic link between increased NOX2-mediated ROS production and modulation of PITX2. Our findings offer insights into possible mechanisms through which obesity triggers AF and support NOX2 inhibition as a potential novel prophylactic or adjunctive therapy for patients with obesity-mediated AF.
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