ArticleBlood2017
Mice with a deficiency in CLEC-2 are protected against deep vein thrombosis.
Article in Blood, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers.
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Who cites it
106 citing papers in PubMed, 183 citations in OpenAlex.
- Molecular control of platelet extravasation into tumors and its impact on tumor growth.Blood vessels, thrombosis & hemostasis · 2026Article
- Platelet CLEC-2 activation leads to GPIb⍺ shedding: Implications for doxorubicin chemotherapy and thrombosis.The Journal of biological chemistry · 2026Article
- Receptor homodimerization significantly prolongs the lifetime of ligand-induced cross-linking of CLEC-2 but not GPVI.Blood vessels, thrombosis & hemostasis · 2026Article
- Mechanobiology of cancer-associated thrombosis: from molecular mechanisms to therapeutic innovation.Journal of nanobiotechnology · 2026Review
- Serum CAPN1 and CLEC2 as Biomarkers for Hearing Loss Severity and Internal Auditory Artery Narrowing in Sudden Sensorineural Hearing Loss.International journal of general medicine · 2026Article
- Cancer-Associated Thrombosis (CAT); mechanisms and treatment options.Thrombosis journal · 2025Review
- Platelet-derived biomimetic nanoplatforms: a promising drug delivery strategy for cardiovascular disease.Journal of nanobiotechnology · 2025Review
- Article
- Metabolic pathways in deep vein thrombosis: a new frontier for therapeutic intervention.Blood · 2025Review
- Discrete and conserved inflammatory signatures drive thrombosis in different organs after Salmonella infection.Nature communications · 2025Article
- Podoplanin and microthrombi in lung injury.Blood vessels, thrombosis & hemostasis · 2025Article
- Knockdown of PDPN in astrocytes reduces hippocampal inflammation in T2DM mice.Frontiers in immunology · 2025Article
- Discovery of Carbonic Anhydrase 9 as a Novel CLEC2 Ligand in a Cellular Interactome Screen.Cells · 2024Article
- Btk inhibition: the importance of being selective.Blood advances · 2024Article
- Selective Btk inhibition by PRN1008/PRN473 blocks human CLEC-2, and PRN473 reduces venous thrombosis formation in mice.Blood advances · 2024Article
- Inhibiting MMP13 Attenuates Deep Vein Thrombosis in a Mouse Model by Reducing the Expression of Pdpn.Current medical science · 2024Article
- C-type lectin-like receptor 2: roles and drug target.Thrombosis journal · 2024Review
- A novel therapy for fracture healing by increasing lymphatic drainage.Journal of orthopaedic translation · 2024Article
- Lymphatic System and the Kidney: From Lymphangiogenesis to Renal Inflammation and Fibrosis Development.International journal of molecular sciences · 2024Review
- Platelet functional abnormalities in pediatric patients with kaposiform hemangioendothelioma/Kasabach-Merritt phenomenon.Blood advances · 2023Article
46 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Deep vein thrombosis (DVT) with its major complication, pulmonary embolism, is a global health problem. Mechanisms of DVT remain incompletely understood. Platelets play a role in DVT, but the impact of specific platelet receptors remains unclear. Platelet C-type lectin-like receptor 2 (CLEC-2) is known to maintain the physiological state of blood vasculature under inflammatory conditions. DVT is a thromboinflammatory disorder developing largely as sterile inflammation in the vessel wall. We hypothesized therefore that CLEC-2 might play a role in DVT. Here, using a murine DVT model of inferior vena cava (IVC) stenosis, we demonstrate that mice with general inducible deletion of CLEC-2 or platelet-specific deficiency in CLEC-2 are protected against DVT. No phenotype in the complete stasis model was observed. Transfusion of wild-type platelets into platelet-specific CLEC-2 knockout mice restored thrombosis. Deficiency in CLEC-2 as well as inhibition of podoplanin, a ligand of CLEC-2, was associated with reduced platelet accumulation at the IVC wall after 6 hours of stenosis. Podoplanin was expressed in the IVC wall, where it was localized in the vicinity of the abluminal side of the endothelium. The level of podoplanin in the IVC increased after 48 hours of stenosis to a substantially higher extent in mice with a thrombus vs those without a thrombus. Treatment of animals with an anti-podoplanin neutralizing antibody resulted in development of smaller thrombi. Thus, we propose a novel mechanism of DVT, whereby CLEC-2 and upregulation of podoplanin expression in the venous wall trigger thrombus formation.
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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.