ArticleBlood2019
Red blood cells modulate structure and dynamics of venous clot formation in sickle cell disease.
Article in Blood, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
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Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.
- Ancestry-independent risk of venous thromboembolism in individuals with sickle cell trait vs factor V Leiden.Blood advances · 2024Pooled it
- Phenome- and laboratory-wide meta-analyses of sickle cell trait reveal multi-system disease associations.American journal of human genetics · 2026Article
- Red blood cell-derived transglutaminase 2 influences thrombus formation.Research and practice in thrombosis and haemostasis · 2026Article
- When sickle cell trait is not just trait: risk of VTE.Hematology. American Society of Hematology. Education Program · 2025Review
- Cellular and molecular mechanisms of thrombosis and thrombus-targeted thrombolytic strategies.Materials today. Bio · 2025Review
- Review
- Red blood cell aggregation within a blood clot causes platelet-independent clot shrinkage.Blood advances · 2025Article
- Addressing the pathophysiology of venous thrombosis and chronic kidney disease in sickle cell trait using a mouse model.Blood advances · 2025Article
- Comparative Proteomic Analysis Reveals Altered Ciliary Proteins in Sickle Cell Disease.Journal of proteome research · 2025Article
- Development and validation of a novel screening tool for deep vein thrombosis in patients with spinal cord injury: A five-year cross-sectional study.Spinal cord · 2024Article
- Associations of RBC counts and incidence of DVT in patients with spinal cord injury: a five year observational retrospective study.Journal of orthopaedic surgery and research · 2024Observational
- CA125-Associated Activated Partial Thromboplastin Time and Thrombin Time Decrease in Patients with Adenomyosis.Journal of multidisciplinary healthcare · 2024Article
- Mouse models of sickle cell disease: Imperfect and yet very informative.Blood cells, molecules & diseases · 2024Review
- Crucial roles of red blood cells and platelets in whole blood thrombin generation.Blood advances · 2023Article
- Sickle red blood cell-derived extracellular vesicles activate endothelial cells and enhance sickle red cell adhesion mediated by von Willebrand factor.British journal of haematology · 2023Article
- Factor XII contributes to thrombotic complications and vaso-occlusion in sickle cell disease.Blood · 2023Article
- The Role of Inflammation in The Cellular and Molecular Mechanisms of Cardiopulmonary Complications of Sickle Cell Disease.Biomolecules · 2023Review
- Moderate hypoxia induces metabolic divergence in circulating monocytes and tissue resident macrophages from Berkeley sickle cell anemia mice.Frontiers in medicine · 2023Article
- Blood clot contraction: Mechanisms, pathophysiology, and disease.Research and practice in thrombosis and haemostasis · 2023Article
- Evidence of protective effects of recombinant ADAMTS13 in a humanized model of sickle cell disease.Haematologica · 2022Article
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19 authors at 2 institutions in 2 countries.
Funding
Abstract
Sickle cell disease (SCD) is associated with chronic activation of coagulation and an increased risk of venous thromboembolism. Erythrocyte sickling, the primary pathologic event in SCD, results in dramatic morphological changes in red blood cells (RBCs) because of polymerization of the abnormal hemoglobin. We used a mouse model of SCD and blood samples from sickle patients to determine if these changes affect the structure, properties, and dynamics of sickle clot formation. Sickling of RBCs and a significant increase in fibrin deposition were observed in venous thrombi formed in sickle mice. During ex vivo clot contraction, the number of RBCs extruded from sickle whole blood clots was significantly reduced compared with the number released from sickle cell trait and nonsickle clots in both mice and humans. Entrapment of sickled RBCs was largely factor XIIIa-independent and entirely mediated by the platelet-free cellular fraction of sickle blood. Inhibition of phosphatidylserine, but not administration of antisickling compounds, increased the number of RBCs released from sickle clots. Interestingly, whole blood, but not plasma clots from SCD patients, was more resistant to fibrinolysis, indicating that the cellular fraction of blood mediates resistance to tissue plasminogen activator. Sickle trait whole blood clots demonstrated an intermediate phenotype in response to tissue plasminogen activator. RBC exchange in SCD patients had a long-lasting effect on normalizing whole blood clot contraction. Furthermore, RBC exchange transiently reversed resistance of whole blood sickle clots to fibrinolysis, in part by decreasing platelet-derived PAI-1. These properties of sickle clots may explain the increased risk of venous thromboembolism observed in SCD.
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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 Socratic graph.