ArticleAntioxidants (Basel, Switzerland)2017
NOX2-Induced Activation of Arginase and Diabetes-Induced Retinal Endothelial Cell Senescence.
Article in Antioxidants (Basel, Switzerland), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
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Who cites it
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.
- Association between the triglyceride glucose index and diabetic retinopathy in type 2 diabetes: a meta-analysis.Frontiers in endocrinology · 2023Pooled it
- The Central Role of Oxidative Stress in Diabetic Retinopathy: Advances in Pathogenesis, Diagnosis, and Therapy.Diagnostics (Basel, Switzerland) · 2026Review
- Targeting Arginase 1 but Not Arginase 2 Protects from Myocardial Ischemia-Reperfusion Injury via Nitric Oxide Signaling by Red Blood Cells in Type 2 Diabetes.Antioxidants (Basel, Switzerland) · 2026Article
- Maternal diabetes programs sexually dimorphic early-onset cardiovascular dysfunction in metabolically healthy offspring.Cell reports. Medicine · 2025Article
- NADPH oxidases: redox regulation of cell homeostasis and disease.Physiological reviews · 2025Review
- The role of microglia in the development of diabetic retinopathy and its potential clinical application.Human cell · 2025Review
- Citrulline Plus Arginine Induces an Angiogenic Response and Increases Permeability in Retinal Endothelial Cells via Nitric Oxide Production.International journal of molecular sciences · 2025Article
- PCSK9 in Vascular Aging and Age-Related Diseases.Aging and disease · 2025Review
- Progress in Nanotechnology for Treating Ocular Surface Chemical Injuries: Reflecting on Advances in Ophthalmology.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Senescent endothelial cells: a potential target for diabetic retinopathy.Angiogenesis · 2024Review
- Pathological high intraocular pressure induces glial cell reactive proliferation contributing to neuroinflammation of the blood-retinal barrier via the NOX2/ET-1 axis-controlled ERK1/2 pathway.Journal of neuroinflammation · 2024Article
- Revolutionizing Diabetic Foot Ulcer Care: The Senotherapeutic Approach.Aging and disease · 2024Review
- Review
- Aging, Cellular Senescence, and Glaucoma.Aging and disease · 2024Review
- Redox Regulation of Immunometabolism in Microglia Underpinning Diabetic Retinopathy.Antioxidants (Basel, Switzerland) · 2024Review
- Investigation of the Effects of a Novel NOX2 Inhibitor, GLX7013170, against Glutamate Excitotoxicity and Diabetes Insults in the Retina.Pharmaceuticals (Basel, Switzerland) · 2024Article
- The multifaceted nature of diabetic erectile dysfunction: uncovering the intricate mechanisms and treatment strategies.Frontiers in endocrinology · 2024Review
- Connecting epigenetics and inflammation in vascular senescence: state of the art, biomarkers and senotherapeutics.Frontiers in genetics · 2024Review
- Cellular senescence and ophthalmic diseases: narrative review.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2023Review
- Research progress on the pathogenesis of diabetic retinopathy.BMC ophthalmology · 2023Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Increases in reactive oxygen species (ROS) and decreases in nitric oxide (NO) have been linked to vascular dysfunction during diabetic retinopathy (DR). Diabetes can reduce NO by increasing ROS and by increasing activity of arginase, which competes with nitric oxide synthase (NOS) for their commons substrate l-arginine. Increased ROS and decreased NO can cause premature endothelial cell (EC) senescence leading to defective vascular repair. We have previously demonstrated the involvement of NADPH oxidase 2 (NOX2)-derived ROS, decreased NO and overactive arginase in DR. Here, we investigated their impact on diabetes-induced EC senescence. Studies using diabetic mice and retinal ECs treated with high glucose or H₂O₂ showed that increases in ROS formation, elevated arginase expression and activity, and decreased NO formation led to premature EC senescence. NOX2 blockade or arginase inhibition prevented these effects. EC senescence was also increased by inhibition of NOS activity and this was prevented by treatment with a NO donor. These results indicate that diabetes/high glucose-induced activation of arginase and decreases in NO bioavailability accelerate EC senescence. NOX2-generated ROS contribute importantly to this process. Blockade of NOX2 or arginase represents a strategy to prevent diabetes-induced premature EC senescence by preserving NO bioavailability.
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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.