ArticleBlood2020
Recognition of PF4-VWF complexes by heparin-induced thrombocytopenia antibodies contributes to thrombus propagation.
Article in Blood, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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.
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Who cites it
39 citing papers in PubMed, 77 citations in OpenAlex.
- Graft-derived VWF drives platelet activation and thrombocytopenia during porcine liver xenotransplantation to brain-dead human recipients.The Journal of clinical investigation · 2026Article
- Using a plastic cannula prevents arteriovenous fistula failure in early cannulation.Renal failure · 2025Article
- Antiphospholipid syndrome (APS) is a platelet factor 4 (PF4)-centric immunothrombotic disorder.bioRxiv : the preprint server for biology · 2025Article
- Platelet factor 4 modulates endothelial cell antimicrobial activity to enhance bacterial clearance and improve sepsis outcomes.bioRxiv : the preprint server for biology · 2025Article
- Reversible Platelet Aggregation Induced by Low-Temperature Storage in Heparinized Whole Blood Samples.Hematology reports · 2025Article
- Endothelial cell activation enhances thromboinflammation in vaccine-induced immune thrombotic thrombocytopenia.Blood advances · 2025Article
- Development of a protease-resistant ADAMTS13 to improve stability against proteolytic degradation.Blood advances · 2025Article
- Review
- Functions for platelet factor 4 (PF4/CXCL4) and its receptors in fibroblast-myofibroblast transition and fibrotic failure of arteriovenous fistulas (AVFs).The journal of vascular access · 2024Article
- Thrombotic anti-PF4 immune disorders: HIT, VITT, and beyond.Hematology. American Society of Hematology. Education Program · 2023Article
- Vaccine-Induced Immune Thrombocytopenia and Thrombosis (VITT)-Insights from Clinical Cases, In Vitro Studies and Murine Models.Journal of clinical medicine · 2023Review
- Treatment of thrombocytopenia and thrombosis in HIT in mice using deglycosylated KKO: a novel therapeutic?Blood advances · 2023Article
- Novel Knowledge about Molecular Mechanisms of Heparin-Induced Thrombocytopenia Type II and Treatment Targets.International journal of molecular sciences · 2023Review
- Article
- New perspectives on the induction and acceleration of immune-associated thrombosis by PF4 and VWF.Frontiers in immunology · 2023Review
- Transcription factors in megakaryocytes and platelets.Frontiers in immunology · 2023Review
- Cardiovascular-related proteomic changes in ECFCs exposed to the serum of COVID-19 patients.International journal of biological sciences · 2023Article
- Vaccine-induced immune thrombotic thrombocytopenia: what do we know hitherto?Frontiers in medicine · 2023Review
- Chemokines, molecular drivers of thromboinflammation and immunothrombosis.Frontiers in immunology · 2023Review
- Mechanisms of ADAMTS13 regulation.Journal of thrombosis and haemostasis : JTH · 2022Review
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Authors and funding
11 authors at 5 institutions in 1 country.
Funding
Abstract
Heparin-induced thrombocytopenia (HIT) is a prothrombotic disorder mediated by complexes between platelet factor 4 (PF4) and heparin or other polyanions, but the risk of thrombosis extends beyond exposure to heparin implicating other PF4 partners. We recently reported that peri-thrombus endothelium is targeted by HIT antibodies, but the binding site(s) has not been identified. We now show that PF4 binds at multiple discrete sites along the surface of extended strings of von Willebrand factor (VWF) released from the endothelium following photochemical injury in an endothelialized microfluidic system under flow. The HIT-like monoclonal antibody KKO and HIT patient antibodies recognize PF4-VWF complexes, promoting platelet adhesion and enlargement of thrombi within the microfluidic channels. Platelet adhesion to the PF4-VWF-HIT antibody complexes is inhibited by antibodies that block FcγRIIA or the glycoprotein Ib-IX complex on platelets. Disruption of PF4-VWF-HIT antibody complexes by drugs that prevent or block VWF oligomerization attenuate thrombus formation in a murine model of HIT. Together, these studies demonstrate assembly of HIT immune complexes along VWF strings released by injured endothelium that might propagate the risk of thrombosis in HIT. Disruption of PF4-VWF complex formation may provide a new therapeutic approach to HIT.
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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.