ArticleJournal of cell science2023
Disturbed flow increases endothelial inflammation and permeability via a Frizzled-4-β-catenin-dependent pathway.
Article in Journal of cell science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 18 citations in OpenAlex.
- Haemodynamic control of zonated liver function via instructive vascular Wnt signalling.Nature communications · 2026Article
- Neurodegeneration-induced angioarchitecture remodeling.Neural regeneration research · 2026Article
- Haemodynamic and biomechanical biomarker analysis of carotid fibromuscular dysplasia via fluid-structure interaction.Biomechanics and modeling in mechanobiology · 2026Article
- Hemodynamic Metrics and Arterial Dysfunction: Insights From a Novel Microfluidic Device.International journal for numerical methods in biomedical engineering · 2026Article
- Mechanosensitive FHL2 tunes endothelial function via microtubule-actomyosin crosstalk.The EMBO journal · 2026Article
- Artificial capillaries-on-a-chip with modular control over lumen size, architecture, and co-culture conditions.Biofabrication · 2026Article
- Exercise-Induced Shear Stress, Endothelial Glycocalyx Remodeling, and Atherosclerotic Plaque Stability: A Mechanistic Review.Journal of cardiovascular development and disease · 2026Review
- Hemadyne: accordion-inspired perfusion for microphysiological systems.Nature communications · 2026Article
- Vascular Endothelial Growth Factor-D Improves Lung Vascular Integrity During Acute Lung Injury.Circulation research · 2026Article
- Ablation of VEGFA following a lumbar intervertebral disc injury attenuates intradiscal neurovascular features and prevents chronic low back pain symptoms.bioRxiv : the preprint server for biology · 2025Article
- Review
- Endothelial protease-activated receptor 4: impotent or important?Frontiers in cardiovascular medicine · 2025Review
- Wnt7a Decreases Brain Endothelial Barrier Function Via β-Catenin Activation.Molecular neurobiology · 2024Article
- Chronic Lymphocytic Leukemia (CLL)-Derived Extracellular Vesicles Educate Endothelial Cells to Become IL-6-Producing, CLL-Supportive Cells.Biomedicines · 2024Article
- Regulation of YAP Promotor Accessibility in Endothelial Mechanotransduction.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Multidirectional or disturbed flow promotes endothelial dysfunction and is associated with early atherogenesis. Here we investigated the role of Wnt signalling in flow-mediated endothelial dysfunction. The expression of Frizzled-4 was higher in cultured human aortic endothelial cells (ECs) exposed to disturbed flow compared to that seen for undisturbed flow, obtained using an orbital shaker. Increased expression was also detected in regions of the porcine aortic arch exposed to disturbed flow. The increased Frizzled-4 expression in cultured ECs was abrogated following knockdown of R-spondin-3. Disturbed flow also increased the nuclear localisation and activation of β-catenin, an effect that was dependent on Frizzled-4 and R-spondin-3. Inhibition of β-catenin using the small-molecule inhibitor iCRT5 or knockdown of Frizzled-4 or R-spondin-3 resulted in reduced expression of pro-inflammatory genes in ECs exposed to disturbed flow, as did inhibition of WNT5A signalling. Inhibition of the canonical Wnt pathway had no effect. Inhibition of β-catenin also reduced endothelial paracellular permeability; this was associated with altered junctional and focal adhesion organisation and cytoskeletal remodelling. These data suggest the presence of an atypical Frizzled-4-β-catenin pathway that promotes endothelial dysfunction in response to disturbed flow.
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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.