ArticleBlood advances2022
Altered fibrin clot structure and dysregulated fibrinolysis contribute to thrombosis risk in severe COVID-19.
Article in Blood advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 64 citations in OpenAlex.
- SARS-CoV-2 spike protein can bind fibrin(ogen), but does not alter plasma fibrin formation, clot structure, or lysis.Blood advances · 2026Article
- SARS-CoV-2 Effects on Respiratory and Neurological Systems: Morphological Findings and Gene Expression in K18-hACE2 Mice Model.Microorganisms · 2026Article
- Coagulopathy in viral haemorrhagic fevers and beyond: molecular mechanisms and targeted interventions.Frontiers in molecular biosciences · 2026Review
- Immunophenotyping of bronchoalveolar lavage and functional impairment in post-COVID syndrome : Insights from a prospective cohort trial.Wiener klinische Wochenschrift · 2025Observational
- From Circulating Biomarkers to Polymorphic Variants: A Narrative Review of Challenges in Thrombophilia Evaluation.Journal of clinical medicine · 2025Review
- Protofibril packing density of individual fibers alters fibrinolysis.Research and practice in thrombosis and haemostasis · 2025Article
- Article
- Patterns of C1-Inhibitor Plasma Levels and Kinin-Kallikrein System Activation in Relation to COVID-19 Severity.Life (Basel, Switzerland) · 2024Article
- Arterial Thrombosis in Acute Respiratory Infections: An Underestimated but Clinically Relevant Problem.Journal of clinical medicine · 2024Review
- Elevated level of extracellular vimentin is associated with an increased fibrin formation potential in sepsis: ex vivo swine study.Intensive care medicine experimental · 2024Article
- Comprehensive Analysis of the Role of Fibrinogen and Thrombin in Clot Formation and Structure for Plasma and Purified Fibrinogen.Biomolecules · 2024Article
- Article
- Flow affects the structural and mechanical properties of the fibrin network in plasma clots.Journal of materials science. Materials in medicine · 2024Article
- Glycosylation signature of plasma IgA of critically ill COVID-19 patients.Frontiers in immunology · 2024Article
- COVID-19: Not a thrombotic disease but a thromboinflammatory disease.Upsala journal of medical sciences · 2024Review
- Effects of inflammation on thrombosis and outcomes in COVID-19: secondary analysis of the ATTACC/ACTIV-4a trial.Research and practice in thrombosis and haemostasis · 2023Article
- Computational Prediction of the Interaction of Ivermectin with Fibrinogen.International journal of molecular sciences · 2023Article
- Thrombus composition and thrombolysis resistance in stroke.Research and practice in thrombosis and haemostasis · 2023Article
- Article
- Fibrin clot properties in cardiovascular disease: from basic mechanisms to clinical practice.Cardiovascular research · 2023Review
Corrections and comments
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Authors and funding
25 authors at 8 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The high incidence of thrombotic events suggests a possible role of the contact system pathway in COVID-19 pathology. In this study, we determined the altered levels of factor XII (FXII) and its activation products in critically ill patients with COVID-19 in comparison with patients with severe acute respiratory distress syndrome related to the influenza virus (acute respiratory distress syndrome [ARDS]-influenza). Compatible with those data, we found rapid consumption of FXII in COVID-19 but not in ARDS-influenza plasma. Interestingly, the lag phase in fibrin formation, triggered by the FXII activator kaolin, was not prolonged in COVID-19, as opposed to that in ARDS-influenza. Confocal and electron microscopy showed that increased FXII activation rate, in conjunction with elevated fibrinogen levels, triggered formation of fibrinolysis-resistant, compact clots with thin fibers and small pores in COVID-19. Accordingly, clot lysis was markedly impaired in COVID-19 as opposed to that in ARDS-influenza. Dysregulated fibrinolytic system, as evidenced by elevated levels of thrombin-activatable fibrinolysis inhibitor, tissue-plasminogen activator, and plasminogen activator inhibitor-1 in COVID-19 potentiated this effect. Analysis of lung tissue sections revealed widespread extra- and intravascular compact fibrin deposits in patients with COVID-19. A compact fibrin network structure and dysregulated fibrinolysis may collectively contribute to a high incidence of thrombotic events in COVID-19.
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