Clinical significance of circulating microparticles in Ph− myeloproliferative neoplasms

Zhou, Wenjuan; Qi, Jiaqian; Zhao, Sihai; Shen, Weihua; Dai, Lingyun; Han, Wei; Huang, Man; Wang, Zhaoyue; Ruan, Changgeng; Wu, Depei; Han, Yue

doi:10.3892/ol.2017.6459

Cited by 39 publications

(39 citation statements)

References 32 publications

(33 reference statements)

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“…48 Among patients with MPNs, serum concentrations of platelet, erythrocyte, and EC microparticles were higher in patients with thrombotic complications ( P <0.05). 48 …”

Section: Thrombosis Risk Factorsmentioning

confidence: 89%

“…46 Among patients with PV, serum microparticles originating from platelets, erythrocytes, granulocytes, and ECs are elevated compared with healthy controls. 47, 48 In particular, patients with MPNs that had the JAK2 V617F mutation had significantly higher plasma concentrations of tissue factor–positive microparticles and erythrocyte microparticles ( P <0.05). 48 Among patients with MPNs, serum concentrations of platelet, erythrocyte, and EC microparticles were higher in patients with thrombotic complications ( P <0.05).…”

Section: Thrombosis Risk Factorsmentioning

confidence: 98%

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Mechanisms of thrombogenesis in polycythemia vera

2015

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Thrombotic and cardiovascular events are among the leading causes of death for patients with polycythemia vera (PV), and thrombosis history is a key criterion for patient risk stratification and treatment strategy. Little is known, however, about mechanisms of thrombogenesis in patients with PV. This report provides an overview of thrombogenesis pathophysiology in patients with PV and elucidates the roles of conventional and nonconventional thrombosis risk factors. In addition to several conventional risk factors for thrombosis, clinical data have implicated increased hematocrit and red blood cell adhesiveness, activated platelets, leukocytosis, and elevated JAK2V617F allele burden in patients with PV. Furthermore, PV-related inflammation may exacerbate thrombogenesis through varied mechanisms, including endothelial damage, inhibition of natural anticoagulant pathways, and secretion of procoagulant factors. These findings suggest a direct link between myeloproliferation and thrombogenesis in PV, which is likely to provide new opportunities for targeted antithrombotic interventions aimed at decreasing PV-related morbidity and mortality.

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“…48 Among patients with MPNs, serum concentrations of platelet, erythrocyte, and EC microparticles were higher in patients with thrombotic complications ( P <0.05). 48 …”

Section: Thrombosis Risk Factorsmentioning

confidence: 89%

Section: Thrombosis Risk Factorsmentioning

confidence: 98%

Mechanisms of thrombogenesis in polycythemia vera

2015

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“…However, while MV production by megakaryocytes is based on a constitutive mechanism, only activated platelets can produce CD62P+ MVs (Flaumenhaft et al , ). High serum levels of MVs have been detected in MF and ET (Caivano et al , ; Zhang et al , ).…”

mentioning

confidence: 99%

Circulating megakaryocyte and platelet microvesicles correlate with response to ruxolitinib and distinct disease severity in patients with myelofibrosis

et al. 2018

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“…However, while MV production by megakaryocytes is based on a constitutive mechanism, only activated platelets can produce CD62P+ MVs (Flaumenhaft et al, 2009). High serum levels of MVs have been detected in MF and ET (Caivano et al, 2015;Zhang et al, 2017).…”

Section: Referencesmentioning

confidence: 99%