ArticleThe Journal of clinical investigation2010
Genetic and cellular evidence of vascular inflammation in neurofibromin-deficient mice and humans.
Article in The Journal of clinical investigation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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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.
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Who cites it
37 citing papers in PubMed, 79 citations in OpenAlex.
- Neurovascular Issues in Neurofibromatosis Type I: Focus on Intracranial Stenosis.Life (Basel, Switzerland) · 2026Review
- Loss of neurofibromin induces inflammatory macrophage phenotypic switch and retinal neovascularization via GLUT1 activation.Cell reports · 2025Article
- ExploringBiomedicines · 2024Review
- The Nf1-Q181X point mutation induces M2 macrophage polarization via the AKT/STAT pathway to promote smooth muscle cell proliferation and migration.Molecular biology reports · 2024Article
- Cerebral arteriopathies of childhood and stroke - A focus on systemic arteriopathies and pediatric fibromuscular dysplasia (FMD).Vascular medicine (London, England) · 2024Review
- Early-life immune activation is a vulnerability factor for adult epileptogenesis in neurofibromatosis type 1 in male mice.Frontiers in neurology · 2024Article
- Risk factors for intraoperative hemorrhage of Type I neurofibromatosis.BMC surgery · 2023Article
- Treatment of celiac artery rupture with a hybrid procedure involving aortic stent grafting and open surgery in a patient with neurofibromatosis type 1.Journal of vascular surgery cases and innovative techniques · 2022Article
- Abnormal peripheral blood cell counts in neurofibromatosis type 1.Scientific reports · 2022Article
- Age-dependent oral manifestations of neurofibromatosis type 1: a case-control study.Orphanet journal of rare diseases · 2022Article
- The NEDD8-activating enzyme inhibitor MLN4924 reduces ischemic brain injury in mice.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- MEK inhibition exerts temporal and myeloid cell-specific effects in the pathogenesis of neurofibromatosis type 1 arteriopathy.Scientific reports · 2021Article
- Desquamative interstitial pneumonia in a non-smoker with neurofibromatosis type 1 (Von Recklinghausen syndrome).BMJ case reports · 2020Article
- Loss of GTPase activating protein neurofibromin stimulates paracrine cell communication via macropinocytosis.Redox biology · 2019Article
- Effector T cell subclasses associate with tumor burden in neurofibromatosis type 1 patients.Cancer immunology, immunotherapy : CII · 2016Article
- Neurofibromin is a novel regulator of Ras-induced reactive oxygen species production in mice and humans.Free radical biology & medicine · 2016Article
- Nf1+/- monocytes/macrophages induce neointima formation via CCR2 activation.Human molecular genetics · 2016Article
- A new horizon of moyamoya disease and associated health risks explored through RNF213.Environmental health and preventive medicine · 2016Review
- Capturing the wide variety of impaired fracture healing phenotypes in Neurofibromatosis Type 1 with eight key factors: a computational study.Scientific reports · 2016Article
- RASopathies: unraveling mechanisms with animal models.Disease models & mechanisms · 2015Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Neurofibromatosis type 1 (NF1) results from mutations in the NF1 tumor suppressor gene, which encodes the protein neurofibromin. NF1 patients display diverse clinical manifestations, including vascular disease, which results from neointima formation and vessel occlusion. However, the pathogenesis of NF1 vascular disease remains unclear. Vessel wall homeostasis is maintained by complex interactions between vascular and bone marrow-derived cells (BMDCs), and neurofibromin regulates the function of each cell type. Therefore, utilizing cre/lox techniques and hematopoietic stem cell transplantation to delete 1 allele of Nf1 in endothelial cells, vascular smooth muscle cells, and BMDCs alone, we determined which cell lineage is critical for neointima formation in vivo in mice. Here we demonstrate that heterozygous inactivation of Nf1 in BMDCs alone was necessary and sufficient for neointima formation after vascular injury and provide evidence of vascular inflammation in Nf1+/- mice. Further, analysis of peripheral blood from NF1 patients without overt vascular disease revealed increased concentrations of inflammatory cells and cytokines previously linked to vascular inflammation and vasoocclusive disease. These data provide genetic and cellular evidence of vascular inflammation in NF1 patients and Nf1+/- mice and provide a framework for understanding the pathogenesis of NF1 vasculopathy and potential therapeutic and diagnostic interventions.
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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.