Mechanisms of Venous Thrombosis and Resolution

Wakefield, Thomas W.; Myers, Daniel D.; Henke, Peter K.

doi:10.1161/atvbaha.108.162289

Cited by 327 publications

(294 citation statements)

References 55 publications

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“…Thrombus formation and resolution in murine models of large-vein thrombosis and in human venous thrombosis involve similar processes, including leukocyte recruitment, both of neutrophils and monocytic cells, activation of the TGF-β pathway, replacement of fibrin and erythrocytes with collagen, vein wall retraction, and neovascularization. 71 Recently, mechanisms of DVT were analyzed with various models in sequence. 21 Intravital 2-photon and epifluorescence microscopic images have shown blood monocytes and neutrophils crawling along and adhering to the venous endothelium, thus initiating DVT.…”

Section: Rate and Sequence Of Thrombus Organization In The Deep Veinsmentioning

confidence: 99%

Coagulation and the Vessel Wall in Pulmonary Embolism

Alias

Lang

2013

Pulm. circ.

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Venous thromboembolism comprises deep-vein thrombosis, thrombus in transit, acute pulmonary embolism, and chronic thromboembolic pulmonary hypertension (CTEPH). Pulmonary thromboemboli commonly resolve, with restoration of normal pulmonary hemodynamics. When they fail to resorb, permanent occlusion of the deep veins and/or CTEPH are the consequences. Apart from endogenous fibrinolysis, venous thrombi resolve by a process of mechanical fragmentation, through organization of the thromboembolus by invasion of endothelial cells, leukocytes, and fibroblasts leading to recanalization. Recent data utilizing various models have contributed to a better understanding of venous thrombosis and the resolution process that is directed at maintaining vascular patency. This review summarizes the plasmatic and cellular components of venous thrombus formation and resolution.

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Section: Rate and Sequence Of Thrombus Organization In The Deep Veinsmentioning

confidence: 99%

Coagulation and the Vessel Wall in Pulmonary Embolism

Alias

Lang

2013

Pulm. circ.

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“…In the context of VTE, a dysfunctional venous endothelium may express increased amounts of von Willebrand factor (vWF), tissue factor (TF), plasminogen activator inhibitor (PAI)-1, and factor V, all of which may promote blood clotting and participate in the development of a thrombus (27). In particular, immunohistochemistry of ilio-femoral veins out autopsy of patients dying of VTE revealed the constant presence of VWF in mural thrombi, and an anti-VWF antibody reduced venous thrombosis in a rabbit VTE model (28).…”

Section: Endothelial Dysfunction and Thrombosismentioning

confidence: 99%

Endothelium, venous thromboembolism and ischaemic cardiovascular events

Gresele

Momi

Migliacci³

2010

Thromb Haemost

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SummaryThe association between venous thromboembolism and arterial thrombosis has emerged as consistent clinical observation in the last few years. While several experimental, epidemiological and pharmacologic studies support this association, the initial pathophysiological mechanism linking these two clinical conditions remains to be established. This review discusses the pathophysiological bases and a number of ex- perimental and clinical observations suggesting that the common link between venous thromboembolism and arterial thrombosis is represented by a dysfunctional endothelium.

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“…Methods for the transformation system and the selection of positive colony were the same as mentioned above. (4). A small amount of plasmid DNA was extracted by QIA-GEN plasmid kit, electrophoresed on a gel and sequenced.…”

Section: Construction Of Recombinant Plasmid Pgl2-basic/5a and Pgl2-bmentioning

confidence: 99%

“…It is widely accepted that vessel wall injury, alterations in the blood flow and blood hypercoagulability are the main causes of DVT formation [1]. Stewart, in the 1970s, proposed that thrombosis was interrelated with inflammation and that thrombosis resolution may be closely linked to vein wall remodelling [4]. To the best of our knowledge, venous thrombi are fibrin-rich and MMPs can degrade extracellular matrix (ECM) components, such as basement collagen, interstitial collagen, fibronectin and various proteoglycans during normal remodelling and repair processes in development and inflammation; they are also responsible for clotting factors, lipoproteins, latent growth factors and chemotactic and cell adhesion molecules [5 - 7].…”

Section: Introductionmentioning

confidence: 99%

MMP-3-1612 polymorphism - a risk factor for deep venous thrombosis formation

Nai-xuan

Sheng

2016

Vasa

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Summary: Background:We investigated the association of the 5A/6A polymorphism in the promoter region at -1612 of the matrix metalloproteinase-3 gene (MMP-3-1612) and deep venous thrombosis (DVT). Patients, materials and methods: The distribution of the MMP-3 (-1612 5A/6A) polymorphism in the case and control groups was detected by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Serum MMP-3 level of two groups was detected using enzyme-linked immunosorbent assay (ELISA). HepG2 cells containing MMP-3-1612 recombinant plasmid were cultured in vitro and the MMP-3 level was defined by luminescence intensity of luciferase. A DVT rat model was built. Serum MMP-3 level in the rats' wounded vein at different time points was detected by ELISA and recorded for investigation of the association between MMP-3 and DVT. Statistical data analysis was conducted with SPSS18.0. Results: On the basis of the observation of MMP-3-1612 genotype frequency and allele frequency in the case and control groups, we identified significantly higher MMP-3-1612 5A allele frequency and higher serum MMP-3 level in the case group than in the control group (both P < 0.05). According to in vitro luciferase measurements, the 5A allele had higher transcriptional activity than the 6A allele. As observed in the rat model, serum MMP-3 level increased with time passing and thrombosis formation after modelling. Conclusions: The MMP-3-1612 5A/6A polymorphism may effect serum MMP-3 level and over-expression of serum MMP-3 level may be a risk factor for DVT formation.

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Mechanisms of Venous Thrombosis and Resolution

Cited by 327 publications

References 55 publications

Coagulation and the Vessel Wall in Pulmonary Embolism

Coagulation and the Vessel Wall in Pulmonary Embolism

Endothelium, venous thromboembolism and ischaemic cardiovascular events

MMP-3-1612 polymorphism - a risk factor for deep venous thrombosis formation

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