ArticleHaematologica2023
Platelet phosphatidylserine is the critical mediator of thrombosis in heparin-induced thrombocytopenia.
Article in Haematologica, 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, 29 citations in OpenAlex.
- Procoagulant platelets: linking coagulation and thromboinflammation in cardiovascular disease.Nature reviews. Cardiology · 2026Review
- On a quest for fingerprints of crystalglobulinemia on platelets and endothelium.Blood vessels, thrombosis & hemostasis · 2026Article
- [Analysis of Clinical Characteristics and Diagnostic Indicators in Patients With Heparin-induced Thrombocytopenia After Cardiac Surgery].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2026Article
- The glycan fingerprint in immune thrombocytopenia.Research and practice in thrombosis and haemostasis · 2026Article
- Bioengineered platelet nanoplatform enables renal-targeted dexamethasone delivery for chronic nephritis therapy with dual anti-inflammatory/anti-fibrotic effects and minimized systemic toxicity.Bioactive materials · 2025Article
- Monoclonal Antibodies in the Pathogenesis of Heparin-Induced Thrombocytopenia.The New England journal of medicine · 2025Article
- Platelet-activating histone/antihistone IgG complexes in anti-PF4-negative thrombosis and thrombocytopenia syndrome.Blood advances · 2025Observational
- Pathophysiological Links Between Inflammatory Bowel Disease and Cardiovascular Disease: The Role of Dysbiosis and Emerging Biomarkers.Biomedicines · 2025Review
- Cardiovascular Toxicity of Metal-Based Nanoparticles.International journal of molecular sciences · 2025Review
- Platelet spleen tyrosine kinase is a key regulator of anti-PF4 antibody-induced immunothrombosis.Blood advances · 2025Article
- Platelet potential to switch to procoagulant phenotype compensates bleeding tendency in patients with hemophilia A.Blood advances · 2025Article
- Imaging flow cytometry as a novel approach for the diagnosis of heparin-induced thrombocytopenia.British journal of haematology · 2025Article
- Beyond platelet activation: dysregulated lipid metabolism in defining risk and pathophysiology of VITT.Research and practice in thrombosis and haemostasis · 2025Article
- Biomedical application of TiOCell biology and toxicology · 2024Article
- An anti-PF4 antibody-related disorder with cerebral venous sinus thrombosis and thrombocytopenia initially presenting as intracranial hemorrhage.Journal of neurology · 2024Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heparin-induced thrombocytopenia (HIT) is a severe immune-mediated prothrombotic disorder caused by antibodies (Ab) reactive to complexes of platelet factor 4 and heparin. Platelets (PLT) and their interaction with different immune cells contribute to prothrombotic conditions in HIT. However, the exact mechanisms and the role of different PLT subpopulations in this prothrombotic environment remain poorly understood. In this study, we observed that HIT patient Ab induce a new PLT population that is characterized by increased P-selectin expression and phosphatidylserine (PS) externalization. Formation of this procoagulant PLT subpopulation was dependent on engagement of PLT Fc-γ-RIIA by HIT Ab and resulted in a significant increase of thrombin generation on the PLT surface. Using an ex vivo thrombosis model and multi-parameter assessment of thrombus formation, we observed that HIT Ab-induced procoagulant PLT propagated formation of large PLT aggregates, leukocyte recruitment and most importantly, fibrin network generation. These prothrombotic conditions were prevented via the upregulation of PLT intracellular cAMP with Iloprost, a clinically approved prostacyclin analogue. Additionally, the functional relevance of P-selectin and PS was dissected. While inhibition of P-selectin did not affect thrombus formation, the specific blockade of PS prevented HIT Ab-mediated thrombin generation and most importantly procoagulant PLT-mediated thrombus formation ex vivo. Taken together, our findings indicate that procoagulant PLT are critical mediators of prothrombotic conditions in HIT. Specific PS targeting could be a promising therapeutic approach to prevent thromboembolic events in HIT patients.
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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.