Fibrin Network Porosity and Endo-/Exogenous Thrombin Cross-talk

He, Shuting; Wallén, Håkan; Thålin, Charlotte; Svensson, Jan; Blombäck, Margareta

doi:10.1055/s-0041-1729963

Cited by 3 publications

(2 citation statements)

References 66 publications

(113 reference statements)

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“…3 ). 28 As early as in 1947, the first report on the structure of fibrin networks within dried collapsed gels using SEM was published by Van Zandt Hawn and Porter 29 ( Fig. 4 ).…”

Section: History Of Fibrin Clot Evaluationmentioning

confidence: 99%

Reviewing the Rich History of Fibrin Clot Research with a Focus on Clinical Relevance

Undas

2024

Semin Thromb Hemost

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Fibrin, described on a single-lens microscopy for the first time by Malpighi in 1666 and named by de Fourcroy, has been extensively studied by biochemists, biophysicists, and more recently by clinicians who recognized that fibrin is the major component of most thrombi. Elucidation of key reactions leading to fibrin clot formation in the 1950s and 1960s grew interest in the clinical relevance of altered fibrin characteristics. Implementation of scanning electron microscopy to image fibrin clots in 1947 and clot permeation studies in the 1970s to evaluate an average pore size enabled plasma clot characterization in cohorts of patients. Unfavorably altered fibrin clot structure was demonstrated by Blombäck's group in coronary artery disease in 1992 and in diabetes in 1996. Fifteen years ago, similar plasma fibrin clot alterations were reported in patients following venous thromboembolism. Multiple myeloma was the first malignant disease to be found to lead to abnormal fibrin clot phenotype in the 1970s. Apart from anticoagulant agents, in 1998, aspirin was first shown to increase fibrin clot permeability in cardiovascular patients. The current review presents key data on the rich history of fibrin research, in particular, those that first documented abnormal fibrin clot properties in a variety of human disease states, as well as factors affecting fibrin phenotype.

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“…3 ). 28 As early as in 1947, the first report on the structure of fibrin networks within dried collapsed gels using SEM was published by Van Zandt Hawn and Porter 29 ( Fig. 4 ).…”

Section: History Of Fibrin Clot Evaluationmentioning

confidence: 99%

Reviewing the Rich History of Fibrin Clot Research with a Focus on Clinical Relevance

Undas

2024

Semin Thromb Hemost

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“…Once thrombin is generated, the process of blood coagulation has reached its final step: thrombin activates fibrinogen to form fibrin monomers, which then polymerize into a network structure ( 74 ). Under normal conditions, the produced fibrin is maintained at normal levels and used for wound healing or hemostasis.…”

Section: Impact Of Covid-19 On Hemostatic Systemmentioning

confidence: 99%

COVID-19: Not a thrombotic disease but a thromboinflammatory disease

He,

Blombäck,

Wallén

2024

ujms

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While Coronavirus Disease in 2019 (COVID-19) may no longer be classified as a global public health emergency, it still poses a significant risk at least due to its association with thrombotic events. This study aims to reaffirm our previous hypothesis that COVID-19 is fundamentally a thrombotic disease. To accomplish this, we have undertaken an extensive literature review focused on assessing the comprehensive impact of COVID-19 on the entire hemostatic system. Our analysis revealed that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection significantly enhances the initiation of thrombin generation. However, it is noteworthy that the thrombin generation may be modulated by specific anticoagulants present in patients’ plasma. Consequently, higher levels of fibrinogen appear to play a more pivotal role in promoting coagulation in COVID-19, as opposed to thrombin generation. Furthermore, the viral infection can stimulate platelet activation either through widespread dissemination from the lungs to other organs or localized effects on platelets themselves. An imbalance between Von Willebrand Factor (VWF) and ADAMTS-13 also contributes to an exaggerated platelet response in this disease, in addition to elevated D-dimer levels, coupled with a significant increase in fibrin viscoelasticity. This paradoxical phenotype has been identified as ‘fibrinolysis shutdown’. To clarify the pathogenesis underlying these hemostatic disorders in COVID-19, we also examined published data, tracing the reaction process of relevant proteins and cells, from ACE2-dependent viral invasion, through induced tissue inflammation, endothelial injury, and innate immune responses, to occurrence of thrombotic events. We therefrom understand that COVID-19 should no longer be viewed as a thrombotic disease solely based on abnormalities in fibrin clot formation and proteolysis. Instead, it should be regarded as a thromboinflammatory disorder, incorporating both classical elements of cellular inflammation and their intricate interactions with the specific coagulopathy.

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Editorial Compilation X

Favaloro

Lippi

2021

Semin Thromb Hemost

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Fibrin Network Porosity and Endo-/Exogenous Thrombin Cross-talk

Cited by 3 publications

References 66 publications

Reviewing the Rich History of Fibrin Clot Research with a Focus on Clinical Relevance

Reviewing the Rich History of Fibrin Clot Research with a Focus on Clinical Relevance

COVID-19: Not a thrombotic disease but a thromboinflammatory disease

Editorial Compilation X

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