ArticleBMC cell biology2017
Intermittent hypoxia causes NOX2-dependent remodeling of atrial connexins.
Article in BMC cell biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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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.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- Role of NADPH oxidase 2-derived reactive oxygen species in cardiac electrophysiological disorders.Channels (Austin, Tex.) · 2026Review
- Oxidative stress and reactive oxygen species in otorhinolaryngological diseases: insights from pathophysiology to targeted antioxidant therapies.Redox report : communications in free radical research · 2025Review
- The relationship between obstructive sleep apnea and atrial remodeling, fibrosis and inflammation.PloS one · 2025Article
- The Role of Ferroptosis in Atrial Fibrillation: A Promising Future.Reviews in cardiovascular medicine · 2024Review
- NADPH Oxidases and Oxidative Stress in the Pathogenesis of Atrial Fibrillation.Antioxidants (Basel, Switzerland) · 2023Review
- Review
- Mouse models of spontaneous atrial fibrillation.Mammalian genome : official journal of the International Mammalian Genome Society · 2023Review
- Identification and Verification of Biomarkers and Immune Infiltration in Obesity-Related Atrial Fibrillation.Biology · 2023Article
- Atrial fibrillation: the role of hypoxia-inducible factor-1-regulated cytokines.Molecular and cellular biochemistry · 2021Review
- Arrhythmias in COVID-19.Methodist DeBakey cardiovascular journal · 2021Review
- ZO-1 Regulates Intercalated Disc Composition and Atrioventricular Node Conduction.Circulation research · 2020Article
- Connexins and Atrial Fibrillation in Obstructive Sleep Apnea.Current sleep medicine reports · 2018Article
- Circulating exosomes in obstructive sleep apnea as phenotypic biomarkers and mechanistic messengers of end-organ morbidity.Respiratory physiology & neurobiology · 2018Review
- Arrhythmogenic Substrates for Atrial Fibrillation in Obesity.Frontiers in physiology · 2018Review
- Anti-arrhythmic Cardiac Phenotype Elicited by Chronic Intermittent Hypoxia Is Associated With Alterations in Connexin-43 Expression, Phosphorylation, and Distribution.Frontiers in endocrinology · 2018Article
- Oxidative stress and inflammation as central mediators of atrial fibrillation in obesity and diabetes.Cardiovascular diabetology · 2017Review
- Predictors of heart rhythm disturbances in hypertensive obese patients with obstructive sleep apnea.Journal of geriatric cardiology : JGC · 2017Article
- Clarifying the Role of Hypoxia in Obstructive Sleep Apnea as a Potential Promulgator of Atrial Fibrillation in Ischemic Stroke.Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine · 2017Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundObstructive sleep apnea has been linked to the development of heart disease and arrhythmias, including atrial fibrillation. Since altered conduction through gap junction channels can contribute to the pathogenesis of such arrhythmias, we examined the abundance and distributions of the major cardiac gap junction proteins, connexin40 (Cx40) and connexin43 (Cx43) in mice treated with sleep fragmentation or intermittent hypoxia (IH) as animal models of the components of obstructive sleep apnea.
resultsWild type C57BL/6 mice or mice lacking NADPH 2 (NOX2) oxidase activity (gp91phox(-/Y)) were exposed to room air or to SF or IH for 6 weeks. Then, the mice were sacrificed, and atria and ventricles were immediately dissected. The abundances of Cx40 or Cx43 in atria and ventricles were unaffected by SF. In contrast, immunoblots showed that the abundance of atrial Cx40 and Cx43 and ventricular Cx43 were reduced in mice exposed to IH. qRT-PCR demonstrated significant reductions of atrial Cx40 and Cx43 mRNAs. Immunofluorescence microscopy revealed that the abundance and size of gap junctions containing Cx40 or Cx43 were reduced in atria by IH treatment of mice. However, no changes of connexin abundance or gap junction size/abundance were observed in IH-treated NOX2-null mice.
conclusionsThese results demonstrate that intermittent hypoxia (but not sleep fragmentation) causes reductions and remodeling of atrial Cx40 and Cx43. These alterations may contribute to the substrate for atrial fibrillation that develops in response to obstructive sleep apnea. Moreover, these connexin changes are likely generated in response to reactive oxygen species generated by NOX2.
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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.