ArticleNature communications2022
JAK2V617F mutation drives vascular resident macrophages toward a pathogenic phenotype and promotes dissecting aortic aneurysm.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 28 papers.
What it found
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 48 citations in OpenAlex.
- CO-Rebreathing in Essential Thrombocythemia and Polycythemia Vera. A Revival of an Old Methodology to Improve Diagnosis and Phlebotomy Decisions.Cancer medicine · 2026Review
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- Association BetweenGenes · 2026Review
- Perivascular mesenchymal cells instruct ST2+ reparative macrophages to promote endovascular injury-induced neointimal hyperplasia in mice.Nature communications · 2026Article
- Prevalence of the JAK2 V617F Mutation in Patients with Non-Cardioembolic Stroke.Journal of atherosclerosis and thrombosis · 2026Article
- Emerging Mechanisms of Abdominal Aortic Aneurysm.Current atherosclerosis reports · 2026Review
- The role of macrophages in aortic physiology and pathophysiology.Frontiers in immunology · 2026Review
- Bridging macro bibliometrics and micro molecular mechanisms: an integrated analysis of global aortic dissection research.Frontiers in cardiovascular medicine · 2026Article
- Polycythemia Vera with Incidental Large Aortic Aneurysm and Giant Cell Arteritis: Case Report.Clinical medicine insights. Case reports · 2026Article
- GSDME-dependent pyroptosis drives abdominal aortic aneurysm via promoting vascular senescence.Nature communications · 2025Article
- Ursodeoxycholic acid alleviates aortic aneurysm and dissection through the intestinal farnesoid X receptor/ceramide synthase 2 axis.Communications biology · 2025Article
- Novel Aortic Dissection Model Links Endothelial Dysfunction and Immune Infiltration.Circulation research · 2025Article
- Myeloid Cells in Abdominal Aortic Aneurysm.Current atherosclerosis reports · 2025Review
- Malignant JAK-signaling: at the interface of inflammation and malignant transformation.Leukemia · 2025Review
- Integrated bioinformatic analysis of immune infiltration and disulfidptosis related gene subgroups in type A aortic dissection.Scientific reports · 2025Article
- Multi-Scale Multi-Cell Computational Model of Inflammation-Mediated Aortic Remodeling in Hypertension.Annals of biomedical engineering · 2025Article
- Myofibrillogenesis Regulator-1 in Smooth Muscle Cells Modulates Inflammation Signaling Pathways via Regulating ROCK1 Ubiquitination and Degradation to Impact Aortic Dissection.Journal of inflammation research · 2025Article
- Single-Cell RNA-Seq Reveals Injuries in Aortic Dissection and Identifies PDGF Signalling Pathway as a Potential Therapeutic Target.Journal of cellular and molecular medicine · 2024Article
- Macrophage polarization and metabolic reprogramming in abdominal aortic aneurysm.Immunity, inflammation and disease · 2024Review
Corrections and comments
- Erratum issued
Authors and funding
27 authors at 6 institutions in 2 countries.
Funding
Abstract
JAK2V617F mutation is associated with an increased risk for athero-thrombotic cardiovascular disease, but its role in aortic disease development and complications remains unknown. In a cohort of patients with myeloproliferative neoplasm, JAK2V617F mutation was identified as an independent risk factor for dilation of both the ascending and descending thoracic aorta. Using single-cell RNA-seq, complementary genetically-modified mouse models, as well as pharmacological approaches, we found that JAK2V617F mutation was associated with a pathogenic pro-inflammatory phenotype of perivascular tissue-resident macrophages, which promoted deleterious aortic wall remodeling at early stages, and dissecting aneurysm through the recruitment of circulating monocytes at later stages. Finally, genetic manipulation of tissue-resident macrophages, or treatment with a Jak2 inhibitor, ruxolitinib, mitigated aortic wall inflammation and reduced aortic dilation and rupture. Overall, JAK2V617F mutation drives vascular resident macrophages toward a pathogenic phenotype and promotes dissecting aortic aneurysm.
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Registered trials
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.