ADAMTS13 and microvascular thrombosis

Tsai, Han‐Mou

doi:10.1586/14779072.4.6.813

Cited by 27 publications

(20 citation statements)

References 80 publications

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“…Compared to healthy controls, patients with PAD showed higher tissue plasminogen activator antigen, plasminogen activator inhibitor-1 antigen, and D-dimer levels both at rest and after treadmill exercise (41). ADAMTS13 is a protease that cleaves VWF, and imbalance between VWF and ADAMTS13 may favor thrombosis (42). In a study of 595 patients with PAD followed for 3 years, 61% of patients who had acute ischemic CV events were compared to 122 PAD controls without events.…”

Section: Markers Of the Thrombosis Cascadementioning

confidence: 99%

Biomarkers and Genetics in Peripheral Artery Disease

Hazarika

Annex

2017

Clinical Chemistry

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BACKGROUND Peripheral artery disease (PAD) is highly prevalent and there is considerable diversity in the initial clinical manifestation and disease progression among individuals. Currently, there is no ideal biomarker to screen for PAD, to risk stratify patients with PAD, or to monitor therapeutic response to revascularization procedures. Advances in human genetics have markedly enhanced the ability to develop novel diagnostic and therapeutic approaches across a host of human diseases, but such developments in the field of PAD are lagging. CONTENT In this article, we will discuss the epidemiology, traditional risk factors for, and clinical presentations of PAD. We will discuss the possible role of genetic factors and gene–environment interactions in the development and/or progression of PAD. We will further explore future avenues through which genetic advances can be used to better our understanding of the pathophysiology of PAD and potentially find newer therapeutic targets. We will discuss the potential role of biomarkers in identifying patients at risk for PAD and for risk stratifying patients with PAD, and novel approaches to identification of reliable biomarkers in PAD. SUMMARY The exponential growth of genetic tools and newer technologies provides opportunities to investigate and identify newer pathways in the development and progression of PAD, and thereby in the identification of newer biomarkers and therapies.

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Section: Markers Of the Thrombosis Cascadementioning

confidence: 99%

Biomarkers and Genetics in Peripheral Artery Disease

Hazarika

Annex

2017

Clinical Chemistry

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“…103 In the absence of additional stimulation, platelets disengage from the vessel wall in a few minutes and return to circulation. Their release is mediated by cleavage of the VWF by the plasma metalloprotease ADAMTS13 (a disintegrin-like and metalloprotease with thrombospondin type I repeats 13), 104 the enzyme that is lacking in thrombotic thrombocytopenic purpura (reviewed in Tsai 105 ). In the absence of this enzyme, the VWF polymers associate in long strings spanning many endothelial cells to which platelets adhere like beads on a necklace.…”

Section: Platelet-vessel Wall Interactionsmentioning

confidence: 99%

The vessel wall and its interactions

Wagner

Frenette²

2008

Blood

318

300

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Historical overviewThe interactions of leukocytes and platelets with the vessel wall, such as occur in inflammation, are highly dynamic and often transient. The development of intravital microscopy was the spark that allowed real-time observations of blood cells in live animals, and led to the detection and molecular analyses of their interactions with the vessel wall. Rudolph Wagner first published in 1839 a description of leukocytes interacting with the vessel wall. 1 In blood vessels of the webbed feet of a grass frog, he observed that leukocytes (then called lymph-corpuscles) in venules were moving in close contact with the vessel wall, and more slowly than other blood cells. The drawing in Figure 1 likely represents the first depiction of rolling leukocytes; we now know that leukocytes roll constitutively in venules of the skin.A few years later the frog-this time its spread tongue-was again central to another milestone microscopic observation. Augustus Waller noted that the trauma caused by the pins and the long exposure to ambient air produced a tongue irritation that triggered the adhesion of lymph-corpuscles onto the vessels of the microcirculation. He also noted that as time passed more of them "escaped" into the surrounding tissue while scarcely any red blood cells (RBCs) could be seen outside the vessel. Waller remarked on "the restorative power of blood which immediately closes the aperture" formed by the extravasating leukocytes and proposed that pus has its origin from these colorless extravasated corpuscles. 2 It took 40 years for defined theories to attempt to explain what initiates these inflammatory responses. In his Lectures on General Pathology, Julius Cohnheim stated "we have here to deal with a molecular change of the vessel walls. . . comprised under the notion and name of inflammation." 3 Cohnheim attributed everything to alterations in the endothelium and noted that inflammatory changes did not affect blood as the vessel wall could be modified even if blood were replaced by saline before ligation. In contrast, at about the same time, Elie Metchnikoff concentrated on "the fundamental importance of phagocytosis in inflammation." In this phagocytic theory of inflammation, he suggested that phagocytes were crucial to destroy the "irritant bodies." 4 Although Metchnikoff stated that "inflammation may occur without any intervention of the blood vessels," he hinted at the need for leukocyte activation as "these cells are in the first place affected by various substances which posses an attraction for them." Clearly, these brilliant scientists were equally right as it is now known that both endothelial and leukocyte activation are key to the inflammatory response.Following vascular injury, the rapid coalescence of blood platelets into forming thrombi was observed by intravital microscopy in the late 1800s (reviewed in Jackson 5 ). The adhesion of platelets to presumably intact but stimulated endothelium was documented only in 1970 by Begent and Born. 6 After ADP application to the outside of a ...

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“…ADAMTS13 (a disintegrin and metalloprotease with thrombospondin type 1 motif, number 13) plays an important role in VWF processing by cleaving the unusually large multimers of VWF originally secreted by endothelial cells and those found contained within platelets (43). A deficiency of ADAMTS13 allows usually large VWF multimers to persist in circulation, resulting in intravascular VWF-platelet aggregation and widespread microvascular thrombosis (44 Figure 3.…”

Section: Dic/modsmentioning

confidence: 99%

Microvascular thrombosis and multiple organ dysfunction syndrome

Gando¹

2010

Critical Care Medicine

281

147

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This paper will review the involvement of disseminated intravascular coagulation-induced microvascular thrombosis in the pathogenesis of multiple organ dysfunction syndrome and the interaction between disseminated intravascular coagulation and systemic inflammatory response syndrome in critically ill patients. The published literature on clinical and experimental studies are the data sources of the study. Histologic evidence of microvascular thrombosis and tissue injury in disseminated intravascular coagulation has been reported in clinical, experimental, and autopsy findings. Proinflammatory cytokine-evoked neutrophil-endothelial activation and interplay between inflammation and coagulation through protease-activated receptors contribute to enhanced microvascular fibrin deposition in organs. In a clinical setting, systemic inflammatory response syndrome and disseminated intravascular coagulation synergistically play pivotal roles in the development of multiple organ dysfunction syndrome and in the poor prognosis of critical illness. Disseminated intravascular coagulation contributes to microvascular thrombosis and subsequent multiple organ dysfunction syndrome. Recent knowledge on the relationship between disseminated intravascular coagulation and systemic inflammatory response syndrome gives further insight into the pathogenic mechanisms of multiple organ dysfunction syndrome in critically ill patients.

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ADAMTS13 and microvascular thrombosis

Cited by 27 publications

References 80 publications

Biomarkers and Genetics in Peripheral Artery Disease

Biomarkers and Genetics in Peripheral Artery Disease

The vessel wall and its interactions

Microvascular thrombosis and multiple organ dysfunction syndrome

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