ArticleScientific reports2020
Nuclear factor kappa B activation in cardiomyocytes by serum of children with obstructive sleep apnea syndrome.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- In Vitro Modelling of Obstructive Sleep Apnea by Intermittent Hypoxia of Human Embryonic Stem Cell-Derived Cardiomyocytes: Expression of ERK1/2, ERK5 and Erbin.International journal of molecular sciences · 2026Article
- Association between body roundness index and obstructive sleep apnea among US adults: data from the 2005-2008 and 2015-2018 National Health and Nutrition Examination Survey.Sleep and biological rhythms · 2025Article
- Effects of obstructive sleep apnea on myocardial injury and dysfunction: a review focused on the molecular mechanisms of intermittent hypoxia.Sleep & breathing = Schlaf & Atmung · 2024Review
- Associations between cardiometabolic phenotypes and levels of TNF-α, CRP, and interleukins in obstructive sleep apnea.Sleep & breathing = Schlaf & Atmung · 2023Article
- Obstructive Sleep Apnea Syndrome In Vitro Model: Controlled Intermittent Hypoxia Stimulation of Human Stem Cells-Derived Cardiomyocytes.International journal of molecular sciences · 2022Article
- The Effect of Sera from Children with Obstructive Sleep Apnea Syndrome (OSAS) on Human Cardiomyocytes Differentiated from Human Embryonic Stem Cells.International journal of molecular sciences · 2021Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Obstructive sleep apnea syndrome (OSA) is associated with cardiovascular morbidity in adults and children. NFκB activity is enhanced in circulating monocytes of adults with OSA, that decreases following positive pressure therapy. OSA children's serum activates NFκB in a cell line. We hypothesized that OSA children's serum can activate NFκB in cardiomyocytes (CM) and effect their viability. In order to explore the role played by NFκB in OSA cardiovascular pathophysiology, rat, mouse and human immortalized CM were exposed to human serum drawn from OSA children and matched controls. Increased expression of NFκB classical subunits p65/p50 as well as major morphological changes occurred in cardiomyocytes following OSA's serum exposure. OSA children's serum induced NFκB activity as measured by p65 nuclear translocation in immortalized human CM and rat cardiomyocytes as well as dense immunostaining of the nucleus. Trypan blue and XTT assays showed that OSA sera induced CM apoptosis. We conclude that NFκB is systemically activated in cardiomyocytes, who also demonstrate decreased viability and contractility following exposure to OSA serum. It supports the hypothesis NFκB plays a role in the evolution of cardiovascular morbidity in OSA. It may support the search for new therapeutic interventions controlling NFκB activation in OSA.
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