ArticleJournal of thrombosis and haemostasis : JTH2020
Endothelial JAK2V617F mutation leads to thrombosis, vasculopathy, and cardiomyopathy in a murine model of myeloproliferative neoplasm.
Article in Journal of thrombosis and haemostasis : JTH, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
- Clonal hematopoiesis of indeterminate potential (CHIP), vascular somatic mutation, and cardiovascular disease: A narrative review.Vascular medicine (London, England) · 2026Review
- CO-Rebreathing in Essential Thrombocythemia and Polycythemia Vera. A Revival of an Old Methodology to Improve Diagnosis and Phlebotomy Decisions.Cancer medicine · 2026Review
- Extensive Cerebral Venous Sinus Thrombosis With Obstructive Hydrocephalus in a Young Female With Underlying Essential Thrombocythemia: A Case Report.Clinical case reports · 2026Article
- Targeting Thrombopoietin/MPL Signaling to Mitigate JAK2V617F-Driven Cardiac Microvascular Disease.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Targeting TPO/MPL Signaling to Mitigate JAK2V617F-driven Cardiac Microvascular Disease.bioRxiv : the preprint server for biology · 2026Article
- Impact of statin use on cardiovascular and hematologic outcomes among patients with myeloproliferative neoplasms.Blood advances · 2026Article
- Clonal hematopoiesis of indeterminate potential: a multisystem hub bridging hematopoietic dysfunction with non-hematopoietic diseases.Military Medical Research · 2025Review
- Distal Internal Carotid Artery Thrombus in Polycythemia Vera.Internal medicine (Tokyo, Japan) · 2025Article
- Repeated Ischemic Stroke due to in situ Thrombus at the Middle Cerebral Artery in a Patient with Essential Thrombocythemia.Internal medicine (Tokyo, Japan) · 2025Article
- Clonal hematopoiesis JAKs up plaque formation.The Journal of clinical investigation · 2025Article
- Endothelial heterogeneity in bone marrow: insights across development, adult life and leukemia.Leukemia · 2025Review
- Portal Vein Thrombosis: State-of-the-Art Review.Journal of clinical medicine · 2024Review
- Prediction of acute coronary syndrome in patients with myeloproliferative neoplasms.Frontiers in cardiovascular medicine · 2024Article
- Clinical Significance of Clonal Hematopoiesis of Indeterminate Potential in Hematology and Cardiovascular Disease.Diagnostics (Basel, Switzerland) · 2022Review
- JAK2V617F-Positive Endothelial Cells Induce Apoptosis and Release JAK2V617F-Positive MicroparticlesTurkish journal of haematology : official journal of Turkish Society of Haematology · 2022Article
- Review
- The possible role of mutated endothelial cells in myeloproliferative neoplasms.Haematologica · 2021Review
- Article
- Thrombotic and hemorrhagic events in 2016 World Health Organization-defined Philadelphia-negative myeloproliferative neoplasm.The Korean journal of internal medicine · 2021Article
- Novel Pathophysiological Mechanisms of Thrombosis in Myeloproliferative Neoplasms.Current hematologic malignancy reports · 2021Review
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
Abstract
objectiveCardiovascular complications are the leading cause of morbidity and mortality in patients with myeloproliferative neoplasms (MPNs). The acquired kinase mutation JAK2V617F plays a central role in these disorders. Mechanisms responsible for cardiovascular dysfunction in MPNs are not fully understood, limiting the effectiveness of current treatment. Vascular endothelial cells (ECs) carrying the JAK2V617F mutation can be detected in patients with MPNs. The goal of this study was to test the hypothesis that the JAK2V617F mutation alters endothelial function to promote cardiovascular complications in patients with MPNs. APPROACH AND
resultsWe employed murine models of MPN in which the JAK2V617F mutation is expressed in specific cell lineages. When JAK2V617F is expressed in both blood cells and vascular ECs, the mice developed MPN and spontaneous, age-related dilated cardiomyopathy with an increased risk of sudden death as well as a prothrombotic and vasculopathy phenotype on histology evaluation. In contrast, despite having significantly higher leukocyte and platelet counts than controls, mice with JAK2V617F-mutant blood cells alone did not demonstrate any cardiac dysfunction, suggesting that JAK2V617F-mutant ECs are required for this cardiovascular disease phenotype. Furthermore, we demonstrated that the JAK2V617F mutation promotes a pro-adhesive, pro-inflammatory, and vasculopathy EC phenotype, and mutant ECs respond to flow shear differently than wild-type ECs.
conclusionsThese findings suggest that the JAK2V617F mutation can alter vascular endothelial function to promote cardiovascular complications in MPNs. Therefore, targeting the MPN vasculature represents a promising new therapeutic strategy for patients with MPNs.
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Registered trials
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