ReviewAntioxidants & redox signaling2011
Flow shear stress and atherosclerosis: a matter of site specificity.
Review in Antioxidants & redox signaling, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 147 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
147 citing papers in PubMed, 1 synthesis or guideline pooled it, 259 citations in OpenAlex.
- Pooled it
- Stent edge vascular response and in-stent geometry after aerobic exercise.Cardiovascular intervention and therapeutics · 2021Trial
- Trial
- Consumption of water containing over 3.5 mg of dissolved hydrogen could improve vascular endothelial function.Vascular health and risk management · 2014Trial
- Polycomb Repressive Complex 2 drives flow-sensitive endothelial states underlying vascular inflammation and disease.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Polymeric anti-platelet carriers for the precision-targeting of age-related cardiovascular and cerebrovascular diseases.Materials today. Bio · 2026Review
- Parent Artery Disease-Related Stroke: What Is the Impact on Endovascular Treatment? A Narrative Review.Journal of clinical medicine · 2026Review
- Targeting mechanosensitive cannabinoid receptor 1 with isoflavone prodrugs attenuates atherosclerotic endothelial dysfunction.Journal of biomedical science · 2026Article
- Mechanosensing of Shear Stress and Uterine Spiral Artery Remodeling by Invasive Trophoblasts in Early Pregnancy.International journal of molecular sciences · 2025Review
- Elevated hydrostatic pressure destabilizes VE-cadherin junctions in a time and shear stress dependent manner: An endothelium-on-chip study.APL bioengineering · 2025Article
- Lats1/2 Are Essential for Developmental Vascular Remodeling and Biomechanical Adaptation to Shear Stress.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Endothelial dysfunction in cardiovascular diseases: mechanisms and in vitro models.Molecular and cellular biochemistry · 2025Review
- Network pharmacology and UPLC/MS/MS metabolic profiling unveil the anti-inflammatory potential of Trifolium alexandrinum.NPJ science of food · 2025Article
- Fluid Shear Stress-Regulated Vascular Remodeling: Past, Present, and Future.Arteriosclerosis, thrombosis, and vascular biology · 2025Review
- High Hcy regulates fluid shear stress pathway activity through histone H3K79 homocysteinylation in hyperhomocysteinemia-related child hypertension.Journal of translational medicine · 2025Article
- Association of Subclavian Steal Phenomenon with Prevalence of Contralateral Vertebral Artery Atherosclerotic Stenosis: A Hospital-Based Cohort Study.Journal of atherosclerosis and thrombosis · 2025Article
- Percutaneous Coronary Intervention for a Chronic Total Occlusion Caused by an External Pacemaker Lead Placement.JACC. Case reports · 2025Article
- Inhibiting MiR-33a-3p Expression Fails to Enhance ApoAI-Mediated Cholesterol Efflux in Pro-Inflammatory Endothelial Cells.Medicina (Kaunas, Lithuania) · 2025Article
- Aortopathy associated with bicuspid aortic valve: advances in clinical and hemodynamics research.Frontiers in physiology · 2025Review
- Flow-Dependent Modulation of Endothelial CaBiomedicines · 2024Article
87 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
It is well accepted that atherosclerosis occurs in a site-specific manner especially at branch points where disturbed blood flow (d-flow) predisposes to the development of plaques. Investigations both in vivo and in vitro have shown that d-flow is pro-atherogenic by promoting oxidative and inflammatory states in the artery wall. In contrast, steady laminar blood flow (s-flow) is atheroprotective by inhibition of oxidative stress and inflammation in the vessel wall. The mechanism for inflammation in endothelial cells (ECs) exposed to d-flow has been well studied and includes redox-dependent activation of apoptosis signal-regulating kinase 1 (ASK1) and Jun NH2-terminal kinase (JNK) that ultimately lead to the expression of adhesive molecules. In contrast, s-flow leads to the activation of the mitogen extracellular-signal-regulated kinase kinase 5/extracellular signal-regulated kinase-5 (MEK5/ERK5) pathway that prevents pro-inflammatory signaling. Important transcriptional events that reflect the pro-oxidant and pro-inflammatory condition of ECs in d-flow include the activation of activator protein 1 (AP-1) and nuclear factor kappaB (NFκB), whereas in s-flow, activation of Krüppel-like factor 2 (KLF2) and nuclear factor erythroid 2-like 2 (Nrf2) are dominant. Recent studies have shown that protein kinase c zeta (PKCζ) is highly activated under d-flow conditions and may represent a molecular switch for EC signaling and gene expression. The targeted modulation of proteins activated in a site-specific manner holds the promise for a new approach to limit atherosclerosis.
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What OpenQuestion holds
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.