Pathogenesis of cardiovascular events in BCR-ABL1-negative myeloproliferative neoplasms.
Animals
Biomarkers
Blood Cells
/ immunology
Blood Coagulation
Blood Coagulation Factors
/ metabolism
Blood Vessels
/ metabolism
Cardiovascular Diseases
/ diagnosis
Disease Management
Disease Models, Animal
Disease Susceptibility
Fusion Proteins, bcr-abl
/ genetics
Hemostasis
Humans
Mutation
Myeloproliferative Disorders
/ complications
Risk Assessment
Risk Factors
Signal Transduction
Thrombosis
/ blood
Journal
Leukemia
ISSN: 1476-5551
Titre abrégé: Leukemia
Pays: England
ID NLM: 8704895
Informations de publication
Date de publication:
04 2021
04 2021
Historique:
received:
08
09
2020
accepted:
28
01
2021
revised:
11
01
2021
pubmed:
5
3
2021
medline:
1
5
2021
entrez:
4
3
2021
Statut:
ppublish
Résumé
Thrombosis, both in arterial and venous territories, is the major complication of myeloproliferative neoplasms and is responsible for a high rate of morbidity and mortality. The currently accepted risk factors are an age over 60 years and a history of thrombosis. However, many complex mechanisms contribute to this increased prothrombotic risk, with involvement of all blood cell types, plasmatic factors, and endothelial cells. Besides, some cardiovascular events may originate from arterial vasospasm that could contribute to thrombotic complications. In this review, we discuss recent results obtained in mouse models in the light of data obtained from clinical studies. We emphasize on actors of thrombosis that are currently not targeted with current therapeutics but could be promising targets, i.e, neutrophil extracellular traps and vascular reactivity.
Identifiants
pubmed: 33658660
doi: 10.1038/s41375-021-01170-z
pii: 10.1038/s41375-021-01170-z
doi:
Substances chimiques
BCR-ABL1 fusion protein, human
0
Biomarkers
0
Blood Coagulation Factors
0
Fusion Proteins, bcr-abl
EC 2.7.10.2
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
935-955Références
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