ArticleBlood2016
High-density lipoprotein modulates thrombosis by preventing von Willebrand factor self-association and subsequent platelet adhesion.
Article in Blood, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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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.
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Who cites it
50 citing papers in PubMed, 90 citations in OpenAlex.
- Mouse models to study von Willebrand factor in thrombosis: a scoping review.Research and practice in thrombosis and haemostasis · 2026Article
- High-density lipoprotein cholesterol: function, dysfunction, and clinical implications.American journal of preventive cardiology · 2026Article
- Von Willebrand factor A1 blockade prevents platelet-mediated sustained occlusion for the treatment of arterial thrombosis.Communications biology · 2026Article
- Elevated levels of apolipoprotein C3 impair platelet function and reduce thrombosis.Journal of thrombosis and haemostasis : JTH · 2026Article
- HDL in Abdominal Aortic Aneurysm: Mechanistic Insight and Therapeutic Potential.Current atherosclerosis reports · 2026Review
- ApoA1/HDL and sepsis-associated vascular endothelial injury: a narrative review.Critical care (London, England) · 2025Review
- Unfolded von Willebrand factor binds protein S and reduces anticoagulant activity.Blood vessels, thrombosis & hemostasis · 2025Article
- Diagnostic value of platelet to high-density lipoprotein cholesterol ratio in abdominal aortic aneurysms.Frontiers in cardiovascular medicine · 2025Article
- Clot or Not? Reviewing the Reciprocal Regulation Between Lipids and Blood Clotting.Arteriosclerosis, thrombosis, and vascular biology · 2024Review
- Von Willebrand factor and hematogenous cancer metastasis under flow.Frontiers in cell and developmental biology · 2024Review
- Article
- Pathway-driven rare germline variants associated with transplant-associated thrombotic microangiopathy (TA-TMA).Thrombosis research · 2023Article
- Type 2B von Willebrand disease mutations differentially perturb autoinhibition of the A1 domain.Blood · 2023Article
- Apolipoprotein A-I, elevated in trauma patients, inhibits platelet activation and decreases clot strength.Platelets · 2022Article
- Coronary Artery Disease and Aortic Valve Stenosis: A Urine Proteomics Study.International journal of molecular sciences · 2022Article
- Reduced Proteolytic Cleavage of von Willebrand Factor Leads to Aortic Valve Stenosis and Load-Dependent Ventricular Remodeling.JACC. Basic to translational science · 2022Article
- Endothelial-derived von Willebrand factor accelerates fibrin clotting within engineered microvessels.Journal of thrombosis and haemostasis : JTH · 2022Article
- Variations in Blood Platelet Proteome and Transcriptome Revealed Altered Expression of Transgelin-2 in Acute Coronary Syndrome Patients.International journal of molecular sciences · 2022Article
- Hydrodynamic Impact on Blood: From Left Ventricular Assist Devices to Artificial Hearts.Arteriosclerosis, thrombosis, and vascular biology · 2022Article
- Single-molecule imaging of von Willebrand factor reveals tension-dependent self-association.Blood · 2021Article
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
The ability of von Willebrand factor (VWF) to initiate platelet adhesion depends on the number of monomers in individual VWF multimers and on the self-association of individual VWF multimers into larger structures. VWF self-association is accelerated by shear stress. We observed that VWF self-association occurs during adsorption of VWF onto surfaces, assembly of secreted VWF into hyperadhesive VWF strings on the endothelial surface, and incorporation of fluid-phase VWF into VWF fibers. VWF adsorption under static conditions increased with increased VWF purity and was prevented by a component of plasma. We identified that component as high-density lipoprotein (HDL) and its major apolipoprotein ApoA-I. HDL and ApoA-I also prevented VWF on the endothelium from self-associating into longer strands and inhibited the attachment of fluid-phase VWF onto vessel wall strands. Platelet adhesion to VWF fibers was reduced in proportion to the reduction in self-associated VWF. In a mouse model of thrombotic microangiopathy, HDL also largely prevented the thrombocytopenia induced by injection of high doses of human VWF. Finally, a potential role for ApoA-I in microvascular occlusion associated with thrombotic thrombocytopenic purpura and sepsis was revealed by the inverse relationship between the concentration of ApoA-I and that of hyperadhesive VWF. These results suggest that interference with VWF self-association would be a new approach to treating thrombotic disorders.
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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.