ArticleCirculation2014
Neurofibromin-deficient myeloid cells are critical mediators of aneurysm formation in vivo.
Article in Circulation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 33 citations in OpenAlex.
- Article
- Loss of neurofibromin induces inflammatory macrophage phenotypic switch and retinal neovascularization via GLUT1 activation.Cell reports · 2025Article
- Radial Artery Pseudoaneurysm With Cutaneous Manifestations in a Patient With Neurofibromatosis Type 1.Cureus · 2025Article
- Intercostal artery aneurysm presenting as a spontaneous hemothorax in a patient with neurofibromatosis.Journal of surgical case reports · 2024Article
- Statins in Children with Neurofibromatosis Type 1: A Systematic Review of Randomized Controlled Trials.Children (Basel, Switzerland) · 2023Review
- Inside and Out.The New England journal of medicine · 2021Article
- Loss of GTPase activating protein neurofibromin stimulates paracrine cell communication via macropinocytosis.Redox biology · 2019Article
- A patient with neurofibromatosis type 1 presenting with bilateral frontal lobe infarctions following anterior communicating artery aneurysm rupture.SAGE open medical case reports · 2019Article
- Neurofibromin Deficiency Induces Endothelial Cell Proliferation and Retinal Neovascularization.Investigative ophthalmology & visual science · 2018Article
- Astragaloside IV Attenuated 3,4-Benzopyrene-Induced Abdominal Aortic Aneurysm by Ameliorating Macrophage-Mediated Inflammation.Frontiers in pharmacology · 2018Article
- Genetic and Epigenetic Regulation of Aortic Aneurysms.BioMed research international · 2017Review
- Neurofibromin is a novel regulator of Ras-induced reactive oxygen species production in mice and humans.Free radical biology & medicine · 2016Article
- Clinical features of subarachnoid hemorrhage in patients with positive cancer history.Journal of neuro-oncology · 2016Observational
- Neurofibromatosis 1-associated panhypopituitarism presenting as hypoglycaemic seizures and stroke-like symptoms.BMJ case reports · 2015Article
Corrections and comments
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Authors and funding
15 authors at 1 institution in 1 country.
Funding
Abstract
backgroundNeurofibromatosis type 1 (NF1) is a genetic disorder resulting from mutations in the NF1 tumor suppressor gene. Neurofibromin, the protein product of NF1, functions as a negative regulator of Ras activity in circulating hematopoietic and vascular wall cells, which are critical for maintaining vessel wall homeostasis. NF1 patients have evidence of chronic inflammation resulting in the development of premature cardiovascular disease, including arterial aneurysms, which may manifest as sudden death. However, the molecular pathogenesis of NF1 aneurysm formation is unknown. METHOD AND
resultsWith the use of an angiotensin II-induced aneurysm model, we demonstrate that heterozygous inactivation of Nf1 (Nf1(+/-)) enhanced aneurysm formation with myeloid cell infiltration and increased oxidative stress in the vessel wall. Using lineage-restricted transgenic mice, we show that loss of a single Nf1 allele in myeloid cells is sufficient to recapitulate the Nf1(+/-) aneurysm phenotype in vivo. Finally, oral administration of simvastatin or the antioxidant apocynin reduced aneurysm formation in Nf1(+/-) mice.
conclusionThese data provide genetic and pharmacological evidence that Nf1(+/-) myeloid cells are the cellular triggers for aneurysm formation in a novel model of NF1 vasculopathy and provide a potential therapeutic target.
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Registered trials
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