ArticleCell & bioscience2024
Revisiting Virchow's triad: exploring the cellular and molecular alterations in cerebral venous congestion.
Article in Cell & bioscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Engineering neurovascular thrombosis: Light-based bioprinting for patient-specific modeling and women's cerebrovascular health.Science advances · 2026Review
- Cerebral Venous Thrombosis: Pathophysiologic Insights, Clinical Evaluation Tools, and Novel Therapeutic Strategies.Diagnostics (Basel, Switzerland) · 2026Review
- Machine learning integration of bulk and single-cell RNA-Seq data reveals COPS2 as a central immune regulator in deep vein thrombosis.American journal of translational research · 2026Article
- Early activation of Virchow's triad in feline hypertrophic cardiomyopathy: beyond spontaneous echo contrast and insights into translational thromboembolism.Frontiers in veterinary science · 2026Review
- Beyond wound closure: translational opportunities and barriers of mesenchymal stem cells and their extracellular vesicles in burn management.Frontiers in cell and developmental biology · 2026Review
- Exploring the association between gut microbiota and venous thromboembolism using a Mendelian randomization analysis.Archives of medical science : AMS · 2026Article
- A rare initial presentation of giant pheochromocytoma: a case report of acute pulmonary embolism complicated by catecholamine-induced cardiomyopathy.Frontiers in oncology · 2026Article
- Immune checkpoint inhibitors and cardiovascular toxicity: immunology, pathophysiology, diagnosis, and management.Journal of thrombosis and thrombolysis · 2025Review
- Molecular mechanisms of endothelial-mesenchymal transition and its pathophysiological feature in cerebrovascular disease.Cell & bioscience · 2025Review
- Hyperfibrinolysis during intra-aortic balloon pump support: a case report on targeted tranexamic acid therapy.Frontiers in cardiovascular medicine · 2025Article
- Cerebral venous disorders: clinical presentation, diagnostic strategy, and contemporary management.Frontiers in neurologyReview
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Authors and funding
11 authors.
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Abstract
backgroundCerebral venous thrombosis (CVT) is a rare but serious condition that can lead to significant morbidity and mortality. Virchow's triad elucidates the role of blood hypercoagulability, blood flow dynamics, and endothelial damage in the pathogenesis of CVT. Cerebral venous congestion (CVC) increases the risk of cerebral venous sinus thrombosis and can lead to recurrent episodes and residual symptoms. However, the precise mechanism by which blood congestion leads to thrombosis remains unclear. Our objective was to investigate the cellular and molecular alterations linked to CVC through analysis of the pathological morphology of venous sinus endothelial cells and transcriptomic profiling.
resultsThis study demonstrated a remarkable correlation between CVC and the phenotypic transformation of endothelial cells from an anticoagulant to a procoagulant state. The findings revealed that cerebral venous stasis results in tortuous dilatation of the venous sinuses, with slow blood flow and elevated pressure in the sinuses and damaged endothelial cells of the retroglenoid and internal jugular vein ligation (JVL) rat model. Mechanistically, analysis of transcriptomic results of cerebral venous sinus endothelial cells showed significant activation of platelet activation, complement and coagulation cascades pathway in the JVL rats. Furthermore, the expression of von Willebrand factor (vWF) and coagulation factor VIII (F8) in the complement and coagulation cascades and Fgg and F2 in the platelet activation was increased in the cerebral venous sinuses of JVL rats than in sham rats, suggesting that endothelial cell injury in the venous sinus induced by CVC has a prothrombotic effect. In addition, endothelial cell damage accelerates coagulation and promotes platelet activation. Significantly, the concentrations of vWF, F2 and F8 in venous sinus blood of patients with internal jugular vein stenosis were higher than in their peripheral blood.
conclusionCollectively, our data suggest that CVC can induce endothelial cell damage, which then exhibits a procoagulant phenotype and ultimately increases the risk of CVT. This research contributes to our understanding of the pathophysiology of CVC associated with procoagulant factors and reexamines the components of Virchow's triad in the context of CVC.
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