ArticleThe Journal of clinical investigation2020
Erythrocyte-derived microvesicles induce arterial spasms in JAK2V617F myeloproliferative neoplasm.
Article in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 2 of them syntheses that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
37 citing papers in PubMed, 2 syntheses or guidelines pooled it, 60 citations in OpenAlex.
- Extracellular vesicles and their effect on vascular haemodynamics: a systematic review.Hypertension research : official journal of the Japanese Society of Hypertension · 2024Pooled it
- Association of clonal hematopoiesis mutations with clinical outcomes: A systematic review and meta-analysis.American journal of hematology · 2022Pooled it
- Targeting Thrombopoietin/MPL Signaling to Mitigate JAK2V617F-Driven Cardiac Microvascular Disease.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Development and Validation of Artificial Intelligence Prediction of Epicardial Coronary Artery Spasm in Patients Without Obstructive Coronary Artery Disease.Diagnostics (Basel, Switzerland) · 2026Article
- Prime time for the use of statins in MPNs: from comorbidity drugs to disease-modifying partners.Blood advances · 2026Review
- Targeting TPO/MPL Signaling to Mitigate JAK2V617F-driven Cardiac Microvascular Disease.bioRxiv : the preprint server for biology · 2026Article
- Enhancing Mitophagy with PEP-1-CAT Attenuates Vascular Inflammation and Atherogenesis in Mice.Inflammation · 2026Article
- Thromboinflammation is associated with high thrombotic risk in patients with newly diagnosed myeloproliferative neoplasms.Leukemia · 2026Article
- Tumorous cholesterol biosynthesis curtails anti-tumor immunity by preventing MTOR-TFEB-mediated lysosomal degradation of CD274/PD-L1.Autophagy · 2025Article
- An update on extracellular vesicles in hematologic disorders: molecular mediators, clinical biomarkers, and emerging therapeutics.Molecular biology reports · 2025Review
- Red blood cell extracellular vesicles: new frontiers in hematological biomarker discovery.Frontiers in medicine · 2025Review
- Exacerbation of thromboinflammation by JAK2V617F mutation worsens the prognosis of cerebral venous sinus thrombosis.Blood advances · 2024Article
- Overview of dyslipidemia and metabolic syndrome in myeloproliferative neoplasms.World journal of clinical oncology · 2024Review
- Review
- Inflammation as a cause of acute myocardial infarction in patients with myeloproliferative neoplasm.World journal of cardiology · 2024Article
- Red Blood Cell Contribution to Thrombosis in Polycythemia Vera and Essential Thrombocythemia.International journal of molecular sciences · 2024Review
- JAK2V617F mutation drives vascular resident macrophages toward a pathogenic phenotype and promotes dissecting aortic aneurysm.Nature communications · 2022Article
- Extracellular Vesicles in Haematological Disorders: A Friend or a Foe?International journal of molecular sciences · 2022Review
- Erythroid lineage Jak2V617F expression promotes atherosclerosis through erythrophagocytosis and macrophage ferroptosis.The Journal of clinical investigation · 2022Article
- Cardiovascular Disease in Myeloproliferative Neoplasms:JACC. CardioOncology · 2022Review
Corrections and comments
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Authors and funding
21 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Arterial cardiovascular events are the leading cause of death in patients with JAK2V617F myeloproliferative neoplasms (MPNs). However, their mechanisms are poorly understood. The high prevalence of myocardial infarction without significant coronary stenosis or atherosclerosis in patients with MPNs suggests that vascular function is altered. The consequences of JAK2V617F mutation on vascular reactivity are unknown. We observe here increased responses to vasoconstrictors in arteries from Jak2V617F mice resulting from a disturbed endothelial NO pathway and increased endothelial oxidative stress. This response was reproduced in WT mice by circulating microvesicles isolated from patients carrying JAK2V617F and by erythrocyte-derived microvesicles from transgenic mice. Microvesicles of other cellular origins had no effect. This effect was observed ex vivo on isolated aortas, but also in vivo on femoral arteries. Proteomic analysis of microvesicles derived from JAK2V617F erythrocytes identified increased expression of myeloperoxidase as the likely mechanism accounting for their effect. Myeloperoxidase inhibition in microvesicles derived from JAK2V617F erythrocytes suppressed their effect on oxidative stress. Antioxidants such as simvastatin and N-acetyl cysteine improved arterial dysfunction in Jak2V617F mice. In conclusion, JAK2V617F MPNs are characterized by exacerbated vasoconstrictor responses resulting from increased endothelial oxidative stress caused by circulating erythrocyte-derived microvesicles. Simvastatin appears to be a promising therapeutic strategy in this setting.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.