ArticleResearch and practice in thrombosis and haemostasis2025
Evaluation of the podoplanin/C-type lectin-like receptor-2 (CLEC-2) pathway as a mediator of platelet and coagulation activation in sickle cell disease.
Article in Research and practice in thrombosis and haemostasis, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- SpEchinoidin, a C-type lectin and a member of an expanded CTL family, is up-regulated by phagocytes in sea urchins responding to immune challenge.Developmental and comparative immunology · 2026Article
- Unique molecular profiling of monocyte responses to a high dose of DENV-NS1 reflected the effect of NS1 on hemostasis.Medical microbiology and immunology · 2026Article
- P-Selectin and Platelet-Monocyte Interaction in Inflammation: Mechanisms, Hypothesis, and Open Questions.Journal of inflammation research · 2026Review
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9 authors.
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Abstract
Background: Sickle cell disease (SCD) is a condition characterized by a prothrombotic state attributed to the simultaneous activation of hemostasis and innate immunity, referred to as thromboinflammation. Previous studies have demonstrated that the podoplanin (PDPN)/C-type lectin-like receptor-2 (CLEC-2) pathway is an emerging and important element of the pathogenesis of conditions in which inflammation and thrombosis coexist, but no data is available regarding its role in SCD. Objectives: To explore the PDPN/CLEC-2 pathway in SCD and correlate it with parameters of disease severity. Methods: Fifty SCD patients (35 with SS genotype; 15 with SC genotype) and 25 healthy individuals were recruited. PDPN and CLEC-2 were assessed for both soluble and surface expression on cells and cell aggregates, along with other classical parameters of hemostasis and platelet activation. An Results: Circulating levels and expression of PDPN and CLEC-2 were higher in patients with SCD, particularly in those with genotype SS. The number of CD41 Conclusion: Our findings suggest that the PDPN/CLEC-2 pathway may play an important role in the pathogenesis of thromboinflammation in SCD, especially in patients with the SS genotype.
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