ArticleThe Laryngoscope2024
Murine Pro-Inflammatory Responses to Acute and Sustained Intermittent Hypoxia: Implications for Obstructive Sleep Apnea Research.
Article in The Laryngoscope, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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.
The trial behind it
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
4 citing papers in PubMed, 7 citations in OpenAlex.
- Obstructive sleep apnea as a modifier of endocrine toxicities associated with immune checkpoint inhibitors in lung cancer.Frontiers in immunology · 2026Review
- Interruption of intermittent hypoxia attenuates the severity of pulmonary fibrosis in male mice.Physiological reports · 2025Article
- Evaluation of SIRT1 Protein Levels and SIRT1/rs7895833 Distributions in Turkish Patients With Obstructive Sleep Apnea.Journal of clinical laboratory analysis · 2025Article
- Efficacy of atomoxetine and oxybutynin in the treatment of pediatric obstructive sleep apnea, a three case report.Frontiers in sleep · 2025Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 2 countries.
Funding
Abstract
objectivesObstructive sleep apnea (OSA) is characterized by chronic systemic inflammation; however, the mechanisms underlying these pathologic consequences are incompletely understood. Our objective was to determine the effects of short- versus long-term exposure to intermittent hypoxia (IH) on pro-inflammatory mediators within vulnerable organs impacted by OSA. STUDY
designExperimental animal study.
methodsA total of 8-10 week old C57BL/6J mice were exposed to normoxic or IH conditions for 7 days (short-term) or 6 weeks (long-term) under 12 h light, 12 h dark cycles. After exposure, multiple tissues were collected over a 24 h period. These tissues were processed and evaluated for gene expression and protein levels of pro-inflammatory mediators from peripheral tissues.
resultsWe observed a global decrease in immune response pathways in the heart, lung, and liver compared with other peripheral organs after short-term exposure to IH. Although there were tissue-specific alterations in the gene expression of pro-inflammatory mediators, with down-regulation in the lung and up-regulation in the heart, we also observed reduced protein levels of pro-inflammatory mediators in the serum, lung, and heart following short-term exposure to IH. Long-term exposure to IH resulted in an overall increase in the levels of inflammatory mediators in the serum, lung, and heart.
conclusionsWe demonstrated novel, longitudinal changes in the inflammatory cascade in a mouse model of OSA. The duration of exposure to IH led to significant variability of inflammatory responses within blood and cardiopulmonary tissues. Our findings further elucidate how inflammatory responses change over the course of the disease in vulnerable organs. LEVEL OF EVIDENCE: NA Laryngoscope, 134:S1-S11, 2024.
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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.