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Updated: Nov 15, 2025

Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells
Published on: February 21, 2018
Pathogenesis of cardiovascular events in BCR-ABL1-negative myeloproliferative neoplasms
Alexandre Guy1,2, Johanne Poisson3,4, Chloe James5,6
1UMR1034, Inserm, Biology of Cardiovascular Diseases, University of Bordeaux, Pessac, France.
Insights
Myeloproliferative neoplasms increase thrombosis risk through complex mechanisms. Novel therapeutic targets include neutrophil extracellular traps and vascular reactivity, offering new treatment avenues.
Area of Science:
- Hematology
- Oncology
- Cardiovascular Medicine
Background:
- Thrombosis is a major complication of myeloproliferative neoplasms (MPNs), leading to significant morbidity and mortality.
- Current risk factors include age >60 and prior thrombosis, but complex mechanisms involving blood cells, plasma factors, and endothelium contribute.
- Arterial vasospasm may also play a role in MPN-related thrombotic events.
Purpose of the Study:
- To review recent findings from mouse models and clinical studies on thrombosis in MPNs.
- To highlight potential novel therapeutic targets beyond current treatments.
- To focus on neutrophil extracellular traps and vascular reactivity as promising targets.
Main Methods:
- Review of recent preclinical data from mouse models.
- Analysis of existing clinical study data.
- Synthesis of information on thrombosis mechanisms in MPNs.
Main Results:
- Multiple blood cell types, plasma factors, and endothelial cells contribute to MPN-associated thrombosis.
- Neutrophil extracellular traps (NETs) and altered vascular reactivity are implicated in thrombotic risk.
- These factors represent potential targets for novel therapeutic strategies.
Conclusions:
- Understanding the multifaceted mechanisms of thrombosis in MPNs is crucial.
- Neutrophil extracellular traps and vascular reactivity are promising, yet untargeted, therapeutic avenues.
- Targeting these novel pathways could improve outcomes for MPN patients.
Abstract:
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.
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