ArticlePloS one2025
The relationship between obstructive sleep apnea and atrial remodeling, fibrosis and inflammation.
Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Review
- Obstructive Sleep Apnoea and Atrial Fibrillation: Current Evidence and Emerging Research Directions.Reviews in cardiovascular medicine · 2026Review
- Alamandine Attenuates Hypoxia-Induced Atrial Fibrosis and Atrial Fibrillation by Involving the YAP/TAZ Pathway.Cardiovascular drugs and therapy · 2026Article
- Electrocardiographic Alterations in Obstructive Sleep Apnea Syndrome: Mechanisms and Clinical Relevance.Life (Basel, Switzerland) · 2026Review
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2 authors.
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Abstract
backgroundObstructive sleep apnea (OSA), characterized by chronic intermittent hypoxia (CIH) is associated with atrial fibrillation. We explored the effects of OSA on atrial remodeling, fibrosis and inflammation, using both clinical and experimental studies.
methodsA total of 105 patients were grouped into control (n = 52), mild to moderate OSA (m-OSA, n = 27), and severe OSA (s-OSA, n = 26) groups. The participants underwent echocardiography and blood tests for interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), collagen type 1 (col-1), and collagen type 3 (col-3). In order to eliminate the interference of obesity, an experimental study was performed using lean mice exposed to CIH.
resultsIn clinical patients, severe OSA featured higher body mass index (BMI) than control (28.12 ± 3.43 versus 24.40 ± 3.56 kg/m2, p < 0.001). Left atrial diameter was significantly higher in s-OSA group than in control group (38.35 ± 4.89 versus 35.39 ± 5.29 mm, P = 0.012). Patients with OSA had higher TNF-α levels than those in the control (P = 0.007). Consistently, plasma IL-1β levels were significantly elevated in the s-OSA and m-OSA groups compared with those in the control group. However, we did not observe significant changes in plasma col-1 and col-3 in patients with OSA. Subgroup analysis of patients with a BMI less than 25 kg/m2 showed that the inflammatory cytokine TNFα is correlated with OSA, rather than with BMI. In animal experiments, using lean mice exposed to IH for 3 weeks, WGA and Masson's staining showed that IH enlarged the atrial myocardium and promoted atrial fibrosis. Atrial mRNA expression of TGFβ、col-1, col-3, IL-6, and TNF-α was significantly elevated after IH exposure.
conclusionOSA, characterized by CIH, was associated with the increased atrial structural remodeling, fibrosis and inflammation.
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