ArticleFrontiers in genetics2015
Contribution of oxidative stress to endothelial dysfunction in hereditary hemorrhagic telangiectasia.
Article in Frontiers in genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
- Use of Antihistamine Drugs in Colitis: A Review.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Hereditary hemorrhagic telangiectasia with pulmonary hypertension: a report of three cases.Journal of thoracic disease · 2025Article
- Article
- Assessment of soluble thrombomodulin and soluble endoglin as endothelial dysfunction biomarkers in seriously ill surgical septic patients: correlation with organ dysfunction and disease severity.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2024Article
- Oxidative stress-induced MMP- and γ-secretase-dependent VE-cadherin processing is modulated by the proteasome and BMP9/10.Scientific reports · 2023Article
- The Role of Endothelial Cells in the Onset, Development and Modulation of Vein Graft Disease.Cells · 2022Review
- Kinetics of Biomarkers of Oxidative Stress in Septic Shock: A Pilot Study.Antioxidants (Basel, Switzerland) · 2022Article
- Drug-Induced Photosensitivity: Clinical Types of Phototoxicity and Photoallergy and Pathogenetic Mechanisms.Frontiers in allergy · 2022Review
- The wHole Story About Fenestrations in LSEC.Frontiers in physiology · 2021Review
- Potential Second-Hits in Hereditary Hemorrhagic Telangiectasia.Journal of clinical medicine · 2020Review
- Potential New Non-Invasive Therapy Using Artificial Oxygen Carriers for Pre-Eclampsia.Journal of functional biomaterials · 2017Review
- The LDL/HDL ratio and atherosclerosis in ankylosing spondylitis.Zeitschrift fur Rheumatologie · 2017Article
- Targeting SOD1 induces synthetic lethal killing in BLM- and CHEK2-deficient colorectal cancer cells.Oncotarget · 2015Article
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Authors and funding
2 authors at 1 institution in 2 countries.
Funding
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Abstract
Oxidative stress causes endothelial dysfunction and is implicated in the pathogenesis of cardiovascular diseases. Our studies suggested that reactive oxygen species (ROS) play a crucial role in hereditary hemorrhagic telangiectasia (HHT) disease, a vascular dysplasia affecting 1 in 5,000-8,000 people. Mutations in endoglin (ENG) and activin receptor-like kinase 1 (ACVRL1) genes are responsible for HHT1 and HHT2 and are associated with arteriovenous malformations. ENG and ACVRL1 interact with endothelial nitric oxide synthase (eNOS) and regulate its activation. Mice heterozygous for these genes (Eng (+/-) and Acvrl1 (+/-)) show reduced ENG or ACVRL1 protein levels in endothelial cells causing eNOS uncoupling, generation of ROS rather than nitric oxide (NO•), leading to impaired NO• mediated vasodilation. ROS production is increased in several organs of Eng (+/-) and Acvrl1 (+/-) mice, including lungs, liver, and colon, affected in HHT. The major source of increased oxidative stress in these tissues is eNOS-derived ROS and not mitochondrial or NADPH oxidase-dependent ROS. Eng (+/-) and Acvrl1 (+/-) mice also develop with age signs of pulmonary arterial hypertension attributable to eNOS-derived ROS, which was preventable by antioxidant treatment. To date, only one pilot study has been carried out in HHT patients, and it showed beneficial effects of antioxidant therapy on epistaxis. We suggest that more clinical studies are warranted to investigate whether antioxidants would prevent, delay or attenuate manifestations of disease in individuals with HHT, based on our experimental data in mouse models.
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