ReviewSleep & breathing = Schlaf & Atmung2020
Effect of chronic intermittent hypoxia on gene expression profiles of rat liver: a better understanding of OSA-related liver disease.
Review in Sleep & breathing = Schlaf & Atmung, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Single-nucleus RNA sequencing uncovers cell type-specific alterations in OSA-related liver injury.Scientific reports · 2026Article
- RNA sequencing reveals circular RNA expression patterns in chronic intermittent hypoxia.Sleep and biological rhythms · 2025Article
- Associations Between Obstructive Sleep Apnea and Metabolic Dysfunction-Associated Fatty Liver Disease: Insights from Comprehensive Mendelian Randomization and Gene Expression Analysis.Nature and science of sleep · 2025Article
- Transcriptomic and Polysomnographic Insights Into Core Signaling Pathways in Obstructive Sleep Apnea.Mediators of inflammation · 2025Article
- The role of ferroptosis in chronic intermittent hypoxia-induced lung injury.BMC pulmonary medicine · 2022Article
- Hyoid bone position as an indicator of severe obstructive sleep apnea.BMC pulmonary medicine · 2022Article
- Disparities in oxygen saturation and hypoxic burden levels in obstructive sleep apnoea patient's response to oral appliance treatment.Journal of oral rehabilitation · 2022Article
- Decreased expression of PPARγ is associated with aortic endothelial cell apoptosis in intermittently hypoxic rats.Sleep & breathing = Schlaf & Atmung · 2021Article
- Untargeted Metabolomic Profiling of Liver in a Chronic Intermittent Hypoxia Mouse Model.Frontiers in physiology · 2021Article
- Transcriptomic Changes of Murine Visceral Fat Exposed to Intermittent Hypoxia at Single Cell Resolution.International journal of molecular sciences · 2020Article
- The role of ferroptosis in chronic intermittent hypoxia-induced liver injury in rats.Sleep & breathing = Schlaf & Atmung · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
purposeObstructive sleep apnea (OSA) and OSA-associated chronic intermittent hypoxia (CIH) have been suggested to be associated with increased risk of liver disease. Little is known about the biological pathophysiology and underlying molecular mechanisms. Here we use whole-genome expression profiling to explore the transcriptomic changes induced by CIH in rat liver.
methodsRats (n = 3) were exposed to CIH for 8 weeks and were compared with rats exposed to normoxia (n = 3). Illumina HiSeq 4000 platform was used to examine differentially expressed genes (DEGs) in the liver between control group and CIH rat model. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to validate DEGs. Biological functions of DEGs were determined by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes.
resultsCompared with control group, 318 genes were identified to be dysregulated in the liver of CIH rat model, with 211genes upregulated and 107 genes downregulated. Bioinformatics analysis showed that these genes were extensively related to various physiologic processes such as hepatic metabolism, apoptotic process, and oxidative stress. 10 genes with 5 upregulated and 5 downregulated were selected and further verified by qRT-PCR.
conclusionsCIH resulted in altered gene expression patterns in the liver of rat. The DEGs were related to various physiological and pathological processes in CIH rat liver. These data provide a better understanding of the mechanisms and underlying molecular changes of OSA-related liver disease.
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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.