ArticleThe American journal of pathology2005
Inhibition of NAD(P)H oxidase activity blocks vascular endothelial growth factor overexpression and neovascularization during ischemic retinopathy.
Article in The American journal of pathology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers.
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Who cites it
109 citing papers in PubMed, 178 citations in OpenAlex.
- NADPH oxidases in immunometabolism and disease pathology: mechanistic networks, pollutant triggers, and therapeutic frontiers.Cellular & molecular immunology · 2026Review
- Beyond Neovascularization: Light Response Deficits in Oxygen-Induced Retinopathy Models.Investigative ophthalmology & visual science · 2026Review
- Transcriptomic Profiling Associates Collagen-Rich Extracellular Matrix With Postoperative Angiogenesis in Moyamoya Disease.Journal of cellular and molecular medicine · 2026Article
- Redox Regulation of Microvascular Physiology and Pathophysiology: Insights into Therapeutic Strategies and Limitations.Antioxidants & redox signaling · 2025Review
- Oxidative stress in pediatric diseases associated with the origin of life and growth and development.Frontiers in cell and developmental biology · 2025Review
- Association of Serum Unsaturated Fatty Acid Patterns with the Risk of Diabetic Nephropathy.Kidney diseases (Basel, Switzerland) · 2024Article
- BH4 supplementation reduces retinal cell death in ischaemic retinopathy.Scientific reports · 2023Article
- Endogenous and Exogenous Regulation of Redox Homeostasis in Retinal Pigment Epithelium Cells: An Updated Antioxidant Perspective.International journal of molecular sciences · 2023Review
- Oxidative stress and epigenetics in ocular vascular aging: an updated review.Molecular medicine (Cambridge, Mass.) · 2023Review
- Protective Effect of NOCells · 2023Article
- Association of Serum Bile Acid and Unsaturated Fatty Acid Profiles with the Risk of Diabetic Retinopathy in Type 2 Diabetic Patients.Diabetes, metabolic syndrome and obesity : targets and therapy · 2023Article
- Specific inhibition of NADPH oxidase 2 modifies chronic epilepsy.Redox biology · 2022Article
- Natural Herbal Medicine as a Treatment Strategy for Myocardial Infarction through the Regulation of Angiogenesis.Evidence-based complementary and alternative medicine : eCAM · 2022Review
- Cellular targets in diabetic retinopathy therapy.World journal of diabetes · 2021Review
- Endothelium-specific deletion of Nox4 delays retinal vascular development and mitigates pathological angiogenesis.Angiogenesis · 2021Article
- Vascular Endothelial Growth Factor Signaling in Models of Oxygen-Induced Retinopathy: Insights Into Mechanisms of Pathology in Retinopathy of Prematurity.Frontiers in pediatrics · 2021Review
- NADPH oxidase-induced oxidative stress in the eyes of hypertensive rats.Molecular vision · 2021Article
- Stress Signal Regulation by Na/K-ATPase As a New Approach to Promote Physiological Revascularization in a Mouse Model of Ischemic Retinopathy.Investigative ophthalmology & visual science · 2020Article
- Acrolein: A Potential Mediator of Oxidative Damage in Diabetic Retinopathy.Biomolecules · 2020Review
- Oxidative Stress Markers and the Retinopathy of Prematurity.Journal of clinical medicine · 2020Review
49 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Because oxidative stress has been strongly implicated in up-regulation of vascular endothelial growth factor (VEGF) expression in ischemic retinopathy, we evaluated the role of NAD(P)H oxidase in causing VEGF overexpression and retinal neovascularization. Dihydroethidium imaging analyses showed increased superoxide formation in areas of retinal neovascularization associated with relative retinal hypoxia in a mouse model for oxygen-induced retinopathy. The effect of hypoxia in stimulating superoxide formation in retinal vascular endothelial cells was confirmed by in vitro chemiluminescence assays. The superoxide formation was blocked by specific inhibitors of NAD(P)H oxidase activity (apocynin, gp91ds-tat) indicating that NAD(P)H oxidase is a major source of superoxide formation. Western blot and immunolocalization analyses showed that retinal ischemia increased expression of the NAD(P)H oxidase catalytic subunit gp91phox, which localized primarily within vascular endothelial cells. Treatment of mice with apocynin blocked ischemia-induced increases in oxidative stress, normalized VEGF expression, and prevented retinal neovascularization. Apocynin and gp91ds-tat also blocked the action of hypoxia in causing increased VEGF expression in vitro, confirming the specific role of NAD(P)H oxidase in hypoxia-induced increases in VEGF expression. In conclusion, NAD(P)H oxidase activity is required for hypoxia-stimulated increases in VEGF expression and retinal neovascularization. Inhibition of NAD(P)H oxidase offers a new therapeutic target for the treatment of retinopathy.
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