ReviewBiorheology2015
Role of fluid shear stress in regulating VWF structure, function and related blood disorders.
Review in Biorheology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 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.
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
54 citing papers in PubMed, 112 citations in OpenAlex.
- Von Willebrand factor A1 blockade prevents platelet-mediated sustained occlusion for the treatment of arterial thrombosis.Communications biology · 2026Article
- All-atom simulations reveal distinct pathways for αCellular and molecular life sciences : CMLS · 2026Article
- Force writes memory: proline isomerization as a molecular memory switch.Biochemical Society transactions · 2025Review
- Vorticity-Facilitated Platelet Aggregation: a High Expansion-Ratio Stenotic Microfluidic Platform Unravels the Role of Complex Flow Dynamics in Arterial Thrombosis.Advanced healthcare materials · 2025Article
- Comparative Proteomic Analysis Reveals Altered Ciliary Proteins in Sickle Cell Disease.Journal of proteome research · 2025Article
- Multiscale simulations that incorporate patient-specific neural network models of platelet calcium signaling predict diverse thrombotic outcomes under flow.PLoS computational biology · 2025Article
- FRET Visualization of High Mechanosensation of von Willebrand Factor to Hydrodynamic Force.Biosensors · 2025Article
- Injury-on-a-chip for modelling microvascular trauma-induced coagulation.Lab on a chip · 2025Article
- Glycosylation changes of vWF in circulating extracellular vesicles to predict depression.Scientific reports · 2024Article
- The pathogenesis of cancer-associated thrombosis.International journal of hematology · 2024Review
- Article
- Anemia, Increased Shear Stress, and the Progression of Aortic Stenosis.JACC. Basic to translational science · 2024Article
- Investigating clot-flow interactions by integrating intravital imaging with in silico modeling for analysis of flow, transport, and hemodynamic forces.Scientific reports · 2024Article
- Cellular Blood Flow Modeling with HemoCell.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Topological damping in an ultrafast giant cell.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Article
- A Clinical-Scale Microfluidic Respiratory Assist Device with 3D Branching Vascular Networks.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- A Multiscale Model for Shear-Mediated Platelet Adhesion Dynamics: Correlating In Silico with In Vitro Results.Annals of biomedical engineering · 2023Article
- Acquired von Willebrand Syndrome in a Patient with Multiple Comorbidities, Including MALT Lymphoma with IgA Monoclonal Gammopathy and Hyperviscosity Syndrome.Internal medicine (Tokyo, Japan) · 2023Article
- Shear-induced acquired von Willebrand syndrome: an accomplice of bleeding events in adults on extracorporeal membrane oxygenation support.Frontiers in cardiovascular medicine · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Von Willebrand factor (VWF) is the largest glycoprotein in blood. It plays a crucial role in primary hemostasis via its binding interaction with platelet and endothelial cell surface receptors, other blood proteins and extra-cellular matrix components. This protein is found as a series of repeat units that are disulfide bonded to form multimeric structures. Once in blood, the protein multimer distribution is dynamically regulated by fluid shear stress which has two opposing effects: it promotes the aggregation or self-association of multiple VWF units, and it simultaneously reduces multimer size by facilitating the force-dependent cleavage of the protein by various proteases, most notably ADAMTS13 (a disintegrin and metalloprotease with thrombospondin type repeats, motif 1 type 13). In addition to these effects, fluid shear also controls the solution and substrate-immobilized structure of VWF, the nature of contact between blood platelets and substrates, and the biomechanics of the GpIbα-VWF bond. These features together regulate different physiological and pathological processes including normal hemostasis, arterial and venous thrombosis, von Willebrand disease, thrombotic thrombocytopenic purpura and acquired von Willebrand syndrome. This article discusses current knowledge of VWF structure-function relationships with emphasis on the effects of hydrodynamic shear, including rapid methods to estimate the nature and magnitude of these forces in selected conditions. It shows that observations made by many investigators using solution and substrate-based shearing devices can be reconciled upon considering the physical size of VWF and the applied mechanical force in these different geometries.
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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.