ArticleMediators of inflammation2019
Oscillatory Shear Stress Induces Oxidative Stress via TLR4 Activation in Endothelial Cells.
Article in Mediators of inflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- Preclinical techniques to investigate exercise training in vascular pathophysiology.American journal of physiology. Heart and circulatory physiology · 2021Pooled it
- Endothelial TLR4 at the Crossroads of Vascular Senescence and Targeted Senotherapeutics.Aging cell · 2026Review
- CIRP Promotes Redox-Inflammatory Endothelial Injury in High-Fat Diet-Fed ApoEAntioxidants (Basel, Switzerland) · 2026Article
- Vascular mechanical forces and vascular diseases.Journal of advanced research · 2026Review
- Multidimensional excavation of the current status and trends of mechanobiology in cardiovascular homeostasis and remodeling within 20 years.Mechanobiology in medicine · 2025Review
- The EZH2 Inhibitor GSK126 Alleviates Thromboinflammation in Deep Vein Thrombosis by Suppressing TLR4 Signaling via H3K27me3 Modulation.Journal of inflammation research · 2025Article
- Interplay between Pro-inflammatory Mediators and Oxidative Stressinvolved Recurrent Chronic Heart Failure in Elderly Patients with Coronary Stents.Current medicinal chemistry · 2025Article
- Vascular Response of Triiodothyronine on Isolated Aortic Rings: Contribution of Redox Mechanisms.Arquivos brasileiros de cardiologia · 2024Article
- Role of the portal system in liver regeneration: From molecular mechanisms to clinical management.Liver research (Beijing, China) · 2024Review
- Effect of reactive oxygen, nitrogen, and sulfur species on signaling pathways in atherosclerosis.Vascular pharmacology · 2024Review
- Disturbed flow regulates protein disulfide isomerase A1 expression via microRNA-204.Frontiers in physiology · 2024Article
- Review
- Atherosclerosis and endothelial mechanotransduction: current knowledge and models for future research.American journal of physiology. Cell physiology · 2023Review
- Article
- Shear stress regulation of nanoparticle uptake in vascular endothelial cells.Regenerative biomaterials · 2023Review
- Review
- Endothelial Mechanosensors for Atheroprone and Atheroprotective Shear Stress Signals.Journal of inflammation research · 2022Review
- Multiple inducers of endothelial NOS (eNOS) dysfunction in sickle cell disease.American journal of hematology · 2021Review
- Oxidative Stress Evaluation in Ischemia Reperfusion Models: Characteristics, Limits and Perspectives.International journal of molecular sciences · 2021Review
- Evaluation of Plaque Characteristics and Inflammation Using Magnetic Resonance Imaging.Biomedicines · 2021Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOscillatory shear stress (OSS) disrupts endothelial homeostasis and promotes oxidative stress, which can lead to atherosclerosis. In atherosclerotic lesions, Toll-like receptor 4 (TLR4) is highly expressed. However, the molecular mechanism by which TLR4 modulates oxidative changes and the cell signaling transudation upon OSS is yet to be determined. METHODS AND
resultsCarotid artery constriction (CAC) surgery and a parallel-plate flow chamber were used to modulate shear stress. The results showed that OSS significantly increased the oxidative burden, and this was partly due to TLR4 activation. OSS activated NOX2 and had no significant influence to NOX1 or NOX4 in endothelial cells (ECs). OSS phosphorylated caveolin-1, promoted its binding with endothelial nitric oxide synthase (eNOS), and resulted in deactivation of eNOS. TLR4 inhibition restored levels of nitric oxide (NO) and superoxide dismutase (SOD) in OSS-exposed cells.
conclusionTLR4 modulates OSS-induced oxidative stress by activating NOX2 and suppressing eNOS.
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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.