ArticleFree radical biology & medicine2016
Neurofibromin is a novel regulator of Ras-induced reactive oxygen species production in mice and humans.
Article in Free radical biology & medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- When and why is surgical revascularization indicated for the treatment of moyamoya syndrome in patients with RASopathies? A systematic review of the literature and a single institute experience.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2018Pooled it
- Loss of neurofibromin induces inflammatory macrophage phenotypic switch and retinal neovascularization via GLUT1 activation.Cell reports · 2025Article
- Molecular insights into genodermatoses: Genetic findings from 43 patients.Archives of dermatological research · 2025Article
- Schwann cells in regeneration and cancer: an epithelial-mesenchymal transition perspective.Open biology · 2025Review
- 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
- [Neurovascular pathology in a patient with neurofibromatosis type 1. Case report].Revista de neurologia · 2024Article
- Chemical genetic screens reveal defective lysosomal trafficking as synthetic lethal with NF1 loss.Journal of cell science · 2024Article
- The Contribution of Oxidative Stress toAntioxidants (Basel, Switzerland) · 2023Review
- The Q181X Point Mutation in Nf1 Induces Cerebral Vessel Stenosis.Neuroscience bulletin · 2023Article
- Moyamoya Vasculopathy in Neurofibromatosis Type 1 Pediatric Patients: The Role of Rare Variants ofCancers · 2023Article
- Base excision repair accessory factors in senescence avoidance and resistance to treatments.Cancer drug resistance (Alhambra, Calif.) · 2022Review
- MEK inhibition exerts temporal and myeloid cell-specific effects in the pathogenesis of neurofibromatosis type 1 arteriopathy.Scientific reports · 2021Article
- Ask-Upmark kidney in a girl with neurofibromatosis type 1.CEN case reports · 2020Article
- Loss of GTPase activating protein neurofibromin stimulates paracrine cell communication via macropinocytosis.Redox biology · 2019Article
- Cysteine-based regulation of redox-sensitive Ras small GTPases.Redox biology · 2019Review
- The Protective Roles of Estrogen ReceptorOxidative medicine and cellular longevity · 2019Article
- Pulmonary hypertension associated with neurofibromatosis type 1.European respiratory review : an official journal of the European Respiratory Society · 2018Review
- Neurofibromin Deficiency Induces Endothelial Cell Proliferation and Retinal Neovascularization.Investigative ophthalmology & visual science · 2018Article
- Whole exome sequencing identifies MRVI1 as a susceptibility gene for moyamoya syndrome in neurofibromatosis type 1.PloS one · 2018Article
- Genetic and Epigenetic Regulation of Aortic Aneurysms.BioMed research international · 2017Review
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 1 country.
Funding
Abstract
Neurofibromatosis type 1 (NF1) predisposes individuals to early and debilitating cardiovascular disease. Loss of function mutations in the NF1 tumor suppressor gene, which encodes the protein neurofibromin, leads to accelerated p21(Ras) activity and phosphorylation of multiple downstream kinases, including Erk and Akt. Nf1 heterozygous (Nf1(+/-)) mice develop a robust neointima that mimics human disease. Monocytes/macrophages play a central role in NF1 arterial stenosis as Nf1 mutations in myeloid cells alone are sufficient to reproduce the enhanced neointima observed in Nf1(+/-) mice. Though the molecular mechanisms underlying NF1 arterial stenosis remain elusive, macrophages are important producers of reactive oxygen species (ROS) and Ras activity directly regulates ROS production. Here, we use compound mutant and lineage-restricted mice to demonstrate that Nf1(+/-) macrophages produce excessive ROS, which enhance Nf1(+/-) smooth muscle cell proliferation in vitro and in vivo. Further, use of a specific NADPH oxidase-2 inhibitor to limit ROS production prevents neointima formation in Nf1(+/-) mice. Finally, mononuclear cells from asymptomatic NF1 patients have increased oxidative DNA damage, an indicator of chronic exposure to oxidative stress. These data provide genetic and pharmacologic evidence that excessive exposure to oxidant species underlie NF1 arterial stenosis and provide a platform for designing novels therapies and interventions.
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Registered trials
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