ArticleJournal of translational medicine2018
Contribution of TLR4 signaling in intermittent hypoxia-mediated atherosclerosis progression.
Article in Journal of translational medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 55 citations in OpenAlex.
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- PFKFB3 Mediated Glycolytic Reprogramming Drives Vascular Endothelial Injury Under Chronic Intermittent Hypoxia.International journal of biological sciences · 2026Article
- Association Between the Malnutrition Status and Adverse Cardiovascular Outcomes in Patients With Obstructive Sleep Apnea and Acute Coronary Syndrome.Journal of the American Heart Association · 2025Article
- Review
- Mechanism of action and therapeutic potential of S100A8/A9 in neuroinflammation and cognitive impairment: From molecular target to clinical application (Review).International journal of molecular medicine · 2025Review
- Antioxidant and Anti-Inflammatory Effects of Bioactive Compounds in Atherosclerosis.International journal of molecular sciences · 2025Review
- Association of Obstructive Sleep Apnea and Nocturnal Hypoxemia With the Circadian Rhythm of Myocardial Infarction.Journal of the American Heart Association · 2025Observational
- Mechanisms of wogonoside in the treatment of atherosclerosis based on network pharmacology, molecular docking, and experimental validation.BMC complementary medicine and therapies · 2025Article
- Mandibular Advancement Devices in Obstructive Sleep Apnea and Its Effects on the Cardiovascular System: A Comprehensive Literature Review.Journal of clinical medicine · 2024Review
- Atherosclerosis and Toll-Like Receptor4 (TLR4), Lectin-Like Oxidized Low-Density Lipoprotein-1 (LOX-1), and Proprotein Convertase Subtilisin/Kexin Type9 (PCSK9).Mediators of inflammation · 2024Review
- Role of sirtuins in attenuating plaque vulnerability in atherosclerosis.Molecular and cellular biochemistry · 2024Review
- Possible genetic cross-talk between Down syndrome and obstructive sleep apnea revealed by transcriptomic analysis.Sleep & breathing = Schlaf & Atmung · 2023Article
- Role of oncostatin-M in ECM remodeling and plaque vulnerability.Molecular and cellular biochemistry · 2023Review
- Pathomorphological Manifestations and the Course of the Cervical Cancer Disease Determined by Variations in theDiagnostics (Basel, Switzerland) · 2023Article
- Microvascular Contributions to Alzheimer Disease Pathogenesis: Is Alzheimer Disease Primarily an Endotheliopathy?Biomolecules · 2023Review
- The role of the gut microbiota in health and cardiovascular diseases.Molecular biomedicine · 2022Review
- Inflammatory Burden and Immunomodulative Therapeutics of Cardiovascular Diseases.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundIntermittent hypoxia (IH), a typical character of obstructive sleep apnea (OSA), is related to atherogenesis. However, the role of IH on atherosclerosis (AS) progression and the mechanisms involved remains poorly understood.
methodsIn the present study, high-fat fed ApoE
resultsCompared with the Sham group, the IH treated group further increased atherosclerotic plaque loads and plaque vulnerability in the aortic sinus. Along with increased TLR4 expression, enhanced NF-κB activation, inflammatory activity and aggravated dyslipidemia were observed in the IH treated group. TLR4 interference partly inhibited IH-mediated AS progression with decreased inflammation and improved cholesterol levels. Similarly, in endothelial cells, hypoxia/reoxygenation exposure has been shown to promote TLR4 expression and activation of proinflammatory TLR4/NF-κB signaling, while TLR4 interference inhibited these effects.
conclusionsWe found that the IH accelerated growth and vulnerability of atherosclerotic plaque, which probably acted by triggering the activation of proinflammatory TLR4/NF-κB signaling. These findings may suggest that IH is a risk factor for vulnerable plaque and provide a new insight into the treatment of OSA-induced AS progression.
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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.