thrombosis/hypoxia

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Hypoxia/Hypoxemia-Induced activation of the procoagulant pathways and the pathogenesis of ischemia-associated thrombosis.

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Although oxygen deprivation has long been associated with triggering of the procoagulant pathway and venous thrombosis, blood hypoxemia and stasis by themselves do not lead to fibrin formation. A pathway is outlined through which diminished levels of oxygen activate the transcription factor early

Genome-Wide Expression Analysis Suggests Hypoxia-Triggered Hyper-Coagulation Leading to Venous Thrombosis at High Altitude.

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Venous thromboembolism (VTE), a multi-factorial disease, is the third most common cardiovascular disease. Established genetic and acquired risk factors are responsible for the onset of VTE. High altitude (HA) also poses as an additional risk factor, predisposing individuals to VTE; however, its

Deep venous thrombosis: The valve cusp hypoxia thesis and its incompatibility with modern orthodoxy.

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The valve cusp hypoxia thesis (VCHT) of the aetiology of deep venous thrombosis (DVT) was adumbrated in this journal in 1977 and fully articulated in 2008, the original hypothesis having been strongly corroborated by experiments published in 1981 and 1984. It presents a unitary account of the

Right-to-left interatrial shunt with hypoxemia caused by a right atrial thrombus.

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A right-to-left shunt in the presence of normal pulmonary artery pressure is an unusual cause of hypoxemia in an adult who has a patent foramen ovale. We report a rare case of such a shunt-the result of a right atrial thrombus that formed in a hypercoagulable patient after placement of an indwelling

Cyclooxygenase-2-linked attenuation of hypoxia-induced pulmonary hypertension and intravascular thrombosis.

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Exogenous prostacyclin is effective in reducing pulmonary vascular resistance in some forms of human pulmonary hypertension (PH). To explore whether endogenous prostaglandins played a similar role in pulmonary hypertension, we examined the effect of deleting cyclooxygenase (COX)-gene isoforms in a

Hypoxia and upregulation of hypoxia-inducible factor 1{alpha} stimulate venous thrombus recanalization.

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OBJECTIVE Angiogenic factors are expressed within thrombus during resolution, but the primary stimulus for neovascularization is unknown. Our aims were to determine whether (1) hypoxia and hypoxia-inducible factor 1α (HIF1α) are induced in resolving thrombus, (2) this stimulates angiogenic factor

Intravascular thrombosis after hypoxia-induced pulmonary hypertension: regulation by cyclooxygenase-2.

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BACKGROUND Pulmonary hypertension induced by chronic hypoxia is characterized by thickening of pulmonary artery walls, elevated pulmonary vascular resistance, and right-heart failure. Prostacyclin analogues reduce pulmonary pressures in this condition; raising the possibility that cycloxygenase-2

Vascular wall hypoxia promotes arterial thrombus formation via augmentation of vascular thrombogenicity.

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Atherosclerotic lesions represent a hypoxic milieu. However, the significance of this milieu in atherothrombosis has not been established. We aimed to assess the hypothesis that vascular wall hypoxia promotes arterial thrombus formation. We examined the relation between vascular wall hypoxia and

Arterial wall hypoxia following thrombosis of the vasa vasorum is an initial lesion in atherosclerosis.

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Pressure on the outside of arteries can cause physical and biochemical changes in the vessel wall of rabbits which are characteristic of atherosclerosis. It is hypothesized that occlusion of the vasa vasorum causes ischaemia of the arterial media which results in smooth muscle cell proliferation and

Upregulation of hypoxia-inducible factor 1 alpha in local vein wall is associated with enhanced venous thrombus resolution.

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BACKGROUND Venous thrombus resolution may be regulated by an angiogenic process that involves the surrounding vein wall. The aims of this study were to determine whether: (i) thrombosis stimulates activation of the angiogenic transcription factor, hypoxia-inducible factor (HIF) 1α, and downstream

Hypoxia - an overlooked trigger for thrombosis in COVID-19 and other critically ill patients

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In a recent publication, GEMELLI against COVID-19 group from Italy demonstrated higher incidence of deep vein thrombosis among non-ICU patients despite pharmacological thromboprophylaxis.¹ They identified traditional risk factors like underlying malignancy and immobility as being

Venous valvular stasis-associated hypoxia and thrombosis: what is the link?

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This review focuses on the role of the venous valves in the genesis of thrombus formation in venous thromboembolic disease (VTE). Clinical VTE and the evidence for the valvular origin of venous thrombosis are reviewed. Virchow's triad is then used as a framework for discussion to approach the

Hypoxia and HIF activation as a possible link between sepsis and thrombosis.

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Risk factors for thrombosis include hypoxia and sepsis, but the mechanisms that control sepsis-induced thrombus formation are incompletely understood. A recent article published in Thrombosis Journal: (i) reviews the role of endothelial cells in the pathogenesis of sepsis-associated microthrombosis;

Activation of NLRP3 inflammasome complex potentiates venous thrombosis in response to hypoxia.

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Venous thromboembolism (VTE), caused by altered hemostasis, remains the third most common cause of mortality among all cardiovascular conditions. In addition to established genetic and acquired risk factors, low-oxygen environments also predispose otherwise healthy individuals to VTE. Although

The stimulation of thrombosis by hypoxia.

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Thrombus formation is increased under conditions of hypoxia in animal models of thrombosis and in human populations, but current therapies for thrombosis do not directly target hypoxia-responsive signaling pathways. The vascular response to hypoxia is controlled primarily by the hypoxia-inducible

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