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Article: Role of von Willebrand factor in vascular disease.

Paulinska, P / Spiel, A / Jilma, B

2009 Volume 29, Issue 1, Page(s) 32–38

Abstract: Plasma levels of von Willebrand factor (VWF) are increased in patients with cardiovascular ... levels are predictive in patients with documented vascular disease. Those patients with increased VWF ... a crucial role in thrombogenesis. This fact has made VWF a promising target for research into new ...

Abstract	Plasma levels of von Willebrand factor (VWF) are increased in patients with cardiovascular risk factors. Various studies aimed to elucidate the relation of VWF with thromboembolic cardiovascular events, ischaemic stroke as well as with peripheral arterial occlusive disease. In the general population, there is only a weak association between VWF levels and future cardiovascular events or stroke. In contrast, VWF levels are predictive in patients with documented vascular disease. Those patients with increased VWF suffer a higher incidence of major adverse cardiac events including death. The extent of the VWF release and its levels independently predict clinical outcome in patients with acute coronary syndromes. Elevated VWF levels have also been observed in patients with atrial fibrillation compared to controls and predict outcome. This may at least in part be attributable to the association of VWF with underlying cardiovascular risk factors. Hence, VWF correlates with Framingham and CHADS stroke risk stratification score and can be used as a marker in patients with AF. However, VWF is not only a predictor; it also plays a crucial role in thrombogenesis. This fact has made VWF a promising target for research into new antiplatelet therapies that specifically inhibit VWF. This review focuses on the role of VWF in ACS, ischaemic stroke and peripheral arterial disease and the relevance of therapeutic interventions targeting VWF for ACS patients.
MeSH term(s)	Arterial Occlusive Diseases/blood ; Binding Sites ; Collagen/metabolism ; Coronary Disease/blood ; Coronary Disease/physiopathology ; Factor VIII/metabolism ; Heparin/metabolism ; Humans ; Platelet Membrane Glycoproteins/metabolism ; Reference Values ; Stroke/blood ; Thrombosis/blood ; Thrombosis/physiopathology ; Vascular Diseases/blood ; von Willebrand Factor/metabolism ; von Willebrand Factor/physiology
Chemical Substances	Platelet Membrane Glycoproteins ; von Willebrand Factor ; Factor VIII (9001-27-8) ; Heparin (9005-49-6) ; Collagen (9007-34-5)
Language	English
Publishing date	2009-01
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	801512-0
ISSN	0720-9355
ISSN	0720-9355
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Role of von Willebrand factor in vascular disease

Paulinska, P. / Spiel, A. / Jilma, B.

Hämostaseologie

2009 Volume 29, Issue 1, Page(s) 32

Language	German
Document type	Article
ZDB-ID	801512-0
ISSN	0720-9355
Database	Current Contents Medicine

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Article: Role of von Willebrand factor in vascular disease

Paulinska, P. / Spiel, A. / Jilma, B.

Hämostaseologie

2009 Volume 29, Issue 01, Page(s) 32–38

Abstract: Plasma levels of von Willebrand factor (VWF) are increased in patients with cardiovascular ... In contrast, VWF levels are predictive in patients with documented vascular disease. Those patients ... it also plays a crucial role in thrombogenesis. This fact has made VWF a promising target for research ...

Abstract	Plasma levels of von Willebrand factor (VWF) are increased in patients with cardiovascular risk factors. Various studies aimed to elucidate the relation of VWF with thrombo - embolic cardiovascular events, ischaemic stroke as well as with peripheral arterial occlusive disease. In the general population, there is only a weak association between VWF levels and future cardiovascular events or stroke. In contrast, VWF levels are predictive in patients with documented vascular disease. Those patients with increased VWF suffer a higher incidence of major adverse cardiac events including death. The extent of the VWF release and its levels independently predict clinical outcome in patients with acute coronary syndromes. Elevated VWF levels have also been observed in patients with atrial fibrillation compared to controls and predict outcome. This may at least in part be attributable to the association of VWF with underlying cardiovascular risk factors. Hence, VWF correlates with Framingham and CHADS stroke risk stratification score and can be used as a marker in patients with AF. However, VWF is not only a predictor; it also plays a crucial role in thrombogenesis. This fact has made VWF a promising target for research into new antiplatelet therapies that specifically inhibit VWF. This review focuses on the role of VWF in ACS, ischaemic stroke and peripheral arterial disease and the relevance of therapeutic interventions targeting VWF for ACS patients.
Keywords	Von Willebrand factor
Language	English
Publishing date	2009-01-01
Publisher	Schattauer GmbH
Publishing place	Stuttgart ; New York
Document type	Article
ZDB-ID	801512-0
ISSN	2567-5761 ; 0720-9355
ISSN (online)	2567-5761
ISSN	0720-9355
DOI	10.1055/s-0037-1616936
Database	Thieme publisher's database

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Article ; Online: The role of von Willebrand factor in hemostasis pathology

Yu. N. Avtaeva / I. S. Melnikov / S. A. Vasiliev / Z. A. Gabbasov

Атеротромбоз, Vol 12, Iss 2, Pp 79-

2023 Volume 102

Abstract: Von Willebrand factor (VWF) is a multimeric plasma glycoprotein present in endothelial cells ... to bleeding, as in von Willebrand disease or Heyde syndrome. Pathological activation of VWF may lead ... from globular to fibrillar. Therefore, VWF plays a key role in cellular hemostasis at high shear rates. Acquired ...

Abstract	Von Willebrand factor (VWF) is a multimeric plasma glycoprotein present in endothelial cells, megakaryocytes, platelets, and connective tissue. It mediates platelet adhesion in small arteries. VWF also binds and protects coagulation factor VIII from degradation. Moreover, VWF is involved in inflammatory response, linking hemostasis and inflammation. VWF multimers and platelets attached to damaged or activated endothelium mediate leukocyte recruitment, facilitating local inflammatory response. At shear rates above 5000 s–1, VWF molecules are capable of hydrodynamic activation that changes their conformation from globular to fibrillar. Therefore, VWF plays a key role in cellular hemostasis at high shear rates. Acquired and inherited disfunction, defective synthesis or increased proteolysis of VWF multimers lead to bleeding, as in von Willebrand disease or Heyde syndrome. Pathological activation of VWF may lead to the development of thrombotic complications of coronary artery disease. COVID-19, especially severe form, is characterized by prothrombotic shift in pulmonary vascular bed. Following endothelial damage, VWF plasma level rises and ADAMTS-13 activity decreases. In patients with COVID-19, a change in the VWF/ADAMTS-13 ratio is associated with an increase in the risk of thromboembolic complications. Therefore, assessment of hydrodynamic activation of VWF under flow conditions may be valuable in fundamental research and laboratory diagnostics.
Keywords	гемостаз ; ишемическая болезнь сердца ; синдром хейда ; covid-19 ; микрофлюидные технологии ; Internal medicine ; RC31-1245
Subject code	610
Language	Russian
Publishing date	2023-01-01T00:00:00Z
Publisher	«REMEDIUM GROUP» Ltd.
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Role of von Willebrand factor in venous thromboembolic disease.

Michels, Alison / Lillicrap, David / Yacob, Michael

JVS-vascular science

2021 Volume 3, Page(s) 17–29

Abstract: ... studied in atherothrombotic disease and inflammation is von Willebrand factor (VWF ... in our population, it is critical to understand the evolving role of VWF in venous disease to guide clinical ... venous thrombosis questions of the strict vascular dichotomy of arterial vs venous. The connection between arterial ...

Abstract	Objective: Evolving evidence of the shared risk factors and pathogenic mechanisms in arterial and venous thrombosis questions of the strict vascular dichotomy of arterial vs venous. The connection between arterial and venous thrombosis has been highlighted by common underlying inflammatory processes, a concept known as thromboinflammatory disease. Using this relationship, we can apply knowledge from arterial disease to better understand and potentially mitigate venous disease. A protein that has been extensively studied in atherothrombotic disease and inflammation is von Willebrand factor (VWF). Because many predisposing and provoking factors of venous thromboembolism (VTE) have been shown to directly modulate VWF levels, it is, perhaps, not surprising that VWF has been highlighted by several recent association studies of patients with VTE. Methods: In the present narrative review, we investigated more deeply the effects of VWF in venous disease by synthesizing the data from clinical studies of deep vein thrombosis of the limbs, pulmonary embolism, portal and cerebral vein thrombosis, and the complications of thrombosis, including post-thrombotic syndrome, venous insufficiency, and chronic thromboembolic pulmonary hypertension. We have also discussed the findings from preclinical studies to highlight novel VWF biochemistry in thrombosis and therapeutics. Results: Across the spectrum of venous thromboembolic disease, we consistently observed that elevated VWF levels conferred an increased risk of VTE and long-term venous complications. We have highlighted important findings from VWF molecular research and have proposed mechanisms by which VWF participates in venous disease. Emerging evidence from preclinical studies might reveal novel targets for thromboinflammatory disease, including specific VWF pathophysiology. Furthermore, we have highlighted the utility of measuring VWF to prognosticate and risk stratify for VTE and its complications. Conclusions: As the prevalence of inflammatory processes, such as aging, obesity, and diabetes increases in our population, it is critical to understand the evolving role of VWF in venous disease to guide clinical decisions and therapeutics.
Language	English
Publishing date	2021-10-07
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2666-3503
ISSN (online)	2666-3503
DOI	10.1016/j.jvssci.2021.08.002
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: The Role of Von Willebrand Factor in the Pathogenesis of Pulmonary Vascular Thrombosis in COVID-19.

Babkina, Anastasiya S / Ostrova, Irina V / Yadgarov, Mikhail Ya / Kuzovlev, Artem N / Grechko, Andrey V / Volkov, Alexey V / Golubev, Arkady M

Viruses

2022 Volume 14, Issue 2

Abstract: The increased plasma levels of von Willebrand factor (VWF) in patients with COVID-19 was reported ... in many studies, and its correlation with disease severity and mortality suggest its important role ... of immunohistochemical reaction for VWF in the pulmonary vascular endothelium when the disease duration was more than 10 ...

Abstract	The increased plasma levels of von Willebrand factor (VWF) in patients with COVID-19 was reported in many studies, and its correlation with disease severity and mortality suggest its important role in the pathogenesis of thrombosis in COVID-19. We performed histological and immunohistochemical studies of the lungs of 29 patients who died from COVID-19. We found a significant increase in the intensity of immunohistochemical reaction for VWF in the pulmonary vascular endothelium when the disease duration was more than 10 days. In the patients who had thrombotic complications, the VWF immunostaining in the pulmonary vascular endothelium was significantly more intense than in nonsurvivors without thrombotic complications. Duration of disease and thrombotic complications were found to be independent predictors of increased VWF immunostaining in the endothelium of pulmonary vessels. We also revealed that bacterial pneumonia was associated with increased VWF staining intensity in pulmonary arterial, arteriolar, and venular endothelium, while lung ventilation was an independent predictor of increased VWF immunostaining in arterial endothelium. The results of the study demonstrated an important role of endothelial VWF in the pathogenesis of thrombus formation in COVID-19.
MeSH term(s)	Adult ; Autopsy ; COVID-19/blood ; COVID-19/complications ; Endothelium, Vascular/immunology ; Female ; Humans ; Immunohistochemistry/methods ; Lung/blood supply ; Lung/pathology ; Male ; Middle Aged ; Pneumonia, Bacterial/immunology ; Pulmonary Embolism ; Severity of Illness Index ; Venous Thrombosis/classification ; Venous Thrombosis/etiology ; Venous Thrombosis/pathology ; von Willebrand Factor/analysis
Chemical Substances	von Willebrand Factor
Language	English
Publishing date	2022-01-21
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2516098-9
ISSN	1999-4915 ; 1999-4915
ISSN (online)	1999-4915
ISSN	1999-4915
DOI	10.3390/v14020211
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Article ; Online: Cardiovascular Diseases Risk Predictors: ABO Blood Groups in a Different Role.

Neshat, Sina / Rezaei, Abbas / Farid, Armita / Javanshir, Salar / Dehghan Niri, Fatemeh / Daneii, Padideh / Heshmat-Ghahdarijani, Kiyan / Sotoudehnia Korani, Setayesh

Cardiology in review

2022 Volume 32, Issue 2, Page(s) 174–179

Abstract: ... increase the risk and severity of these conditions by increasing von Willebrand factor and plasma ... with an increased risk and severity of coronary artery disease and acute coronary syndromes. Non-O blood groups ... Blood groups also affect the prognosis of coronary artery disease and acute coronary syndrome and can alter ...

Abstract	Cardiovascular diseases (CVDs) pose a serious threat to people's health, with extremely high global morbidity, mortality, and disability rates. This study aimed to review the literature that examined the relationship between blood groups and CVD. Many studies have reported that non-O blood groups are associated with an increased risk and severity of coronary artery disease and acute coronary syndromes. Non-O blood groups increase the risk and severity of these conditions by increasing von Willebrand factor and plasma cholesterol levels and inducing endothelial dysfunction and inflammation. They have also been linked with increased coronary artery calcification, coronary lesion complexity, and poor collateral circulation. Blood groups also affect the prognosis of coronary artery disease and acute coronary syndrome and can alter the rate of complications and mortality. Several cardiovascular complications have been described for coronavirus disease 2019, and blood groups can influence their occurrence. No studies have found a significant relationship between the Lewis blood group and CVD. In conclusion, people with non-O blood groups should be vigilantly monitored for cardiovascular risk factors as prevention and proper treatment of these risk factors may mitigate their risk of CVD and adverse cardiovascular events.
MeSH term(s)	Humans ; Cardiovascular Diseases/epidemiology ; Cardiovascular Diseases/etiology ; Coronary Artery Disease/epidemiology ; ABO Blood-Group System ; Risk Factors ; Acute Coronary Syndrome
Chemical Substances	ABO Blood-Group System
Language	English
Publishing date	2022-10-27
Publishing country	United States
Document type	Review ; Journal Article
ZDB-ID	1294965-6
ISSN	1538-4683 ; 1061-5377
ISSN (online)	1538-4683
ISSN	1061-5377
DOI	10.1097/CRD.0000000000000463
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Article ; Online: COVID-19 promotes endothelial dysfunction and thrombogenicity: role of proinflammatory cytokines/SGLT2 prooxidant pathway.

Journal of thrombosis and haemostasis : JTH

2023 Volume 22, Issue 1, Page(s) 286–299

Abstract: ... platelet adhesion and aggregation, von Willebrand factor secretion, and thrombin generation. The stimulatory effect ... Although cytokines have a predominant role in endothelium damage, the precise molecular mechanisms are far from being ... tumor necrosis factor-α, monocyte chemoattractant protein-1, and soluble intercellular adhesion molecule-1 were observed ...

Abstract	Background: COVID-19 is associated with an increased risk of cardiovascular complications. Although cytokines have a predominant role in endothelium damage, the precise molecular mechanisms are far from being elucidated. Objectives: The present study hypothesized that inflammation in patients with COVID-19 contributes to endothelial dysfunction through redox-sensitive SGLT2 overexpression and investigated the protective effect of SGLT2 inhibition by empagliflozin. Methods: Human plasma samples were collected from patients with acute, subacute, and long COVID-19 (n = 100), patients with non-COVID-19 and cardiovascular risk factors (n = 50), and healthy volunteers (n = 25). Porcine coronary artery endothelial cells (ECs) were incubated with plasma (10%). Protein expression levels were determined using Western blot analyses and immunofluorescence staining, mRNA expression by quantitative reverse transcription-polymerase chain reaction, and the level of oxidative stress by dihydroethidium staining. Platelet adhesion, aggregation, and thrombin generation were determined. Results: Increased plasma levels of interleukin (IL)-1β, IL-6, tumor necrosis factor-α, monocyte chemoattractant protein-1, and soluble intercellular adhesion molecule-1 were observed in patients with COVID-19. Exposure of ECs to COVID-19 plasma with high cytokines levels induced redox-sensitive upregulation of SGLT2 expression via proinflammatory cytokines IL-1β, IL-6, and tumor necrosis factor-α which, in turn, fueled endothelial dysfunction, senescence, NF-κB activation, inflammation, platelet adhesion and aggregation, von Willebrand factor secretion, and thrombin generation. The stimulatory effect of COVID-19 plasma was blunted by neutralizing antibodies against proinflammatory cytokines and empagliflozin. Conclusion: In patients with COVID-19, proinflammatory cytokines induced a redox-sensitive upregulation of SGLT2 expression in ECs, which in turn promoted endothelial injury, senescence, platelet adhesion, aggregation, and thrombin generation. SGLT2 inhibition with empagliflozin appeared as an attractive strategy to restore vascular homeostasis in COVID-19.
MeSH term(s)	Animals ; Humans ; COVID-19/metabolism ; Cytokines/metabolism ; Endothelial Cells/metabolism ; Inflammation/metabolism ; Intercellular Adhesion Molecule-1/metabolism ; Interleukin-1beta/metabolism ; Interleukin-6/metabolism ; Post-Acute COVID-19 Syndrome ; Reactive Oxygen Species/metabolism ; Sodium-Glucose Transporter 2/metabolism ; Sodium-Glucose Transporter 2/pharmacology ; Swine ; Thrombin/metabolism ; Tumor Necrosis Factor-alpha/metabolism ; Vascular Diseases
Chemical Substances	Cytokines ; empagliflozin (HDC1R2M35U) ; Intercellular Adhesion Molecule-1 (126547-89-5) ; Interleukin-1beta ; Interleukin-6 ; Reactive Oxygen Species ; Sodium-Glucose Transporter 2 ; Thrombin (EC 3.4.21.5) ; Tumor Necrosis Factor-alpha ; SLC5A2 protein, human
Language	English
Publishing date	2023-10-04
Publishing country	England
Document type	Journal Article
ZDB-ID	2112661-6
ISSN	1538-7836 ; 1538-7933
ISSN (online)	1538-7836
ISSN	1538-7933
DOI	10.1016/j.jtha.2023.09.022
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Zs.A 5805: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Role of the coagulation system in the pathogenesis of sickle cell disease.

Nasimuzzaman, Md / Malik, Punam

Blood advances

2019 Volume 3, Issue 20, Page(s) 3170–3180

Abstract: ... downstream of thrombin, such as the tissue factor-FX complex, fibrinogen, platelets, von Willebrand factor ... pathophysiology. The key coagulation factor, thrombin (factor IIa [FIIa]), is both a central protease ... FXII, high-molecular-weight kininogen, etc, also play important roles in SCD pathogenesis ...

Abstract	Sickle cell disease (SCD) is an inherited monogenic red blood cell disorder affecting millions worldwide. SCD causes vascular occlusions, chronic hemolytic anemia, and cumulative organ damage such as nephropathy, pulmonary hypertension, pathologic heart remodeling, and liver necrosis. Coagulation system activation, a conspicuous feature of SCD that causes chronic inflammation, is an important component of SCD pathophysiology. The key coagulation factor, thrombin (factor IIa [FIIa]), is both a central protease in hemostasis and thrombosis and a key modifier of inflammation. Pharmacologic or genetic reduction of circulating prothrombin in Berkeley sickle mice significantly improves survival, ameliorates vascular inflammation, and results in markedly reduced end-organ damage. Accordingly, factors both upstream and downstream of thrombin, such as the tissue factor-FX complex, fibrinogen, platelets, von Willebrand factor, FXII, high-molecular-weight kininogen, etc, also play important roles in SCD pathogenesis. In this review, we discuss the various aspects of coagulation system activation and their roles in the pathophysiology of SCD.
MeSH term(s)	Anemia, Sickle Cell/blood ; Anemia, Sickle Cell/complications ; Anemia, Sickle Cell/etiology ; Blood Coagulation ; Blood Coagulation Factors/metabolism ; Disease Susceptibility ; Humans
Chemical Substances	Blood Coagulation Factors
Language	English
Publishing date	2019-10-25
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2915908-8
ISSN	2473-9537 ; 2473-9529
ISSN (online)	2473-9537
ISSN	2473-9529
DOI	10.1182/bloodadvances.2019000193
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Article ; Online: Role of Endothelial Cells in Acute and Chronic Thrombosis.

Bochenek, Magdalena L / Schäfer, Katrin

Hamostaseologie

2019 Volume 39, Issue 2, Page(s) 128–139

Abstract: ... coagulation, such as thrombomodulin or RNase1. Upon activation, endothelial cells expose von Willebrand factor ... platelet activation and blood coagulation. Endothelial cells play a crucial role in all of these processes and are ... plays an important role for thrombus resolution, whereas failure to completely resolve thrombi ...

Abstract	Haemostasis encompasses a set of strictly regulated actions, such as vasoconstriction, platelet activation and blood coagulation. Endothelial cells play a crucial role in all of these processes and are an integral part of the vascular response to injury resulting in thrombus formation. Healthy endothelium expresses mediators to prevent platelet activation, including prostacyclin and nitric oxide, and to inhibit coagulation, such as thrombomodulin or RNase1. Upon activation, endothelial cells expose von Willebrand factor, integrins and other receptors to interact with activated platelets, erythrocytes and coagulation factors, respectively, resulting in blood clot formation. The endothelial cell response to cytokines and growth factors released from activated platelets and immune cells abundantly present in arterial and venous thrombi also plays an important role for thrombus resolution, whereas failure to completely resolve thrombi may initiate fibrotic remodelling and chronic vascular occlusion both in the arterial and venous tree. Therefore, endothelial cells are increasingly recognized as potential target to prevent thrombotic events and to accelerate thrombus resolution. Here, we discuss recent publications from our group in the context of other studies on the role of the endothelium during acute and chronic thrombotic events.
MeSH term(s)	Acute Disease ; Blood Coagulation/drug effects ; Chronic Disease ; Endothelial Cells/drug effects ; Endothelial Cells/pathology ; Fibrinolytic Agents/pharmacology ; Fibrinolytic Agents/therapeutic use ; Humans ; Thrombosis/drug therapy ; Thrombosis/pathology ; Thrombosis/physiopathology
Chemical Substances	Fibrinolytic Agents
Language	English
Publishing date	2019-01-08
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	801512-0
ISSN	2567-5761 ; 0720-9355
ISSN (online)	2567-5761
ISSN	0720-9355
DOI	10.1055/s-0038-1675614
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