ArticleThe Journal of clinical investigation2017
Endothelial antigen assembly leads to thrombotic complications in heparin-induced thrombocytopenia.
Article in The Journal of clinical investigation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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.
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Who cites it
28 citing papers in PubMed, 57 citations in OpenAlex.
- Sepsis-induced immunothrombosis: from cellular crosstalk to multiple organ dysfunction.Frontiers in immunology · 2026Review
- Endo-chip laser-induced thrombus formation: a vessel-on-chip model for in vitro testing of antithrombotic agents.Blood vessels, thrombosis & hemostasis · 2025Article
- Endothelial cell activation enhances thromboinflammation in vaccine-induced immune thrombotic thrombocytopenia.Blood advances · 2025Article
- Article
- Structural and functional changes underlying activation of monocytes in heparin-induced thrombocytopenia.Journal of thrombosis and haemostasis : JTH · 2025Article
- Glycosaminoglycans: Participants in Microvascular Coagulation of Sepsis.Thrombosis and haemostasis · 2024Review
- Thioredoxin-related transmembrane protein 1 negatively regulates coagulation and phosphatidylserine exposure.Research and practice in thrombosis and haemostasis · 2024Article
- Hemostasis-on-a-chip / incorporating the endothelium in microfluidic models of bleeding.Platelets · 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
- Neutrophil extracellular traps and heparin-induced antibodies contribute to vascular access thrombosis in hemodialysis patients.Kidney research and clinical practice · 2021Article
- Complement mediates binding and procoagulant effects of ultralarge HIT immune complexes.Blood · 2021Article
- Heparin-Induced Thrombocytopenia: A Review of New Concepts in Pathogenesis, Diagnosis, and Management.Journal of clinical medicine · 2021Review
- Quantitative and Qualitative Platelet Derangements in Cardiac Surgery and Extracorporeal Life Support.Journal of clinical medicine · 2021Review
- Bioactivity effects of extracellular matrix proteins on apical papilla cells.Journal of applied oral science : revista FOB · 2021Article
- Heparin-Induced Thrombocytopenia: A Focus on Thrombosis.Arteriosclerosis, thrombosis, and vascular biology · 2021Review
- Elucidation of Cellular Contributions to Heparin-Induced Thrombocytopenia Using Omic Approaches.Frontiers in pharmacology · 2021Review
- COVID-19 versus HIT hypercoagulability.Thrombosis research · 2020Review
- Pathogenesis of heparin-induced thrombocytopenia.Translational research : the journal of laboratory and clinical medicine · 2020Review
- Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Heparin-induced thrombocytopenia (HIT) is a prothrombotic disorder initiated by antibodies against complexes between human platelet factor 4 (hPF4) and heparin. A better understanding of the events that initiate the prothrombotic state may improve approaches to antithrombotic management. Here, we visualized thrombus formation in an in vivo murine model and an endothelialized microfluidic system that simulate the pathogenesis of HIT. hPF4 released from platelets predominantly bound to peri-injury endothelium and formed HIT antigenic complexes that were dissociated by heparin. In mice expressing both hPF4+ and human platelet IgG Fc receptor IIA (FcγRIIA), infusion of the HIT-like monoclonal antibody KKO increased fibrin and platelet deposition at sites of injury, followed immediately by antigen formation on proximate endothelial cells. After a few minutes, HIT antigen was detected within the thrombus itself at the interface between the platelet core and the surrounding shell. We observed similar results in the humanized, endothelialized microfluidic system. hPF4 and KKO selectively bound to photochemically injured endothelium at sites where surface glycocalyx was reduced. These studies support the concept that the perithrombus endothelium is the predominant site of HIT antigen assembly. This suggests that disrupting antigen formation along the endothelium or protecting the endothelium may provide a therapeutic opportunity to prevent thrombotic complications of HIT, while sparing systemic hemostatic pathways.
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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.