ArticlePloS one2018
The novel NADPH oxidase 4 selective inhibitor GLX7013114 counteracts human islet cell death in vitro.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 72 citations in OpenAlex.
- The paracrine signalling between endothelial and pancreatic β-cells: implications for oxidative stress and diabetes.Journal of endocrinological investigation · 2026Review
- Overcoming Oxidative Stress in Parkinson's Disease: NADPH Oxidase 4 (NOX4) as a Potential Therapeutic Target.Antioxidants (Basel, Switzerland) · 2026Review
- Role of NADPH Oxidases as Novel Therapeutic Targets for the Impaired Neurovascular Unit in the Early Stage of Diabetic Retinopathy.International journal of molecular sciences · 2026Review
- Expression, localization and regulation of NADPH oxidases in pancreatic beta cells.Redox report : communications in free radical research · 2025Article
- Functionalized bacterial cellulose membranes with controlled biodegradation and β-estradiol delivery properties for potential intrauterine adhesion prevention.Journal of materials science. Materials in 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
- Design of Benzyl-triazolopyrimidine-Based NADPH Oxidase Inhibitors Leads to the Discovery of a Potent Dual Covalent NOX2/MAOB Inhibitor.Journal of medicinal chemistry · 2025Article
- Delineating the NOX-Mediated Promising Therapeutic Strategies for the Management of Various Cardiovascular Disorders: A Comprehensive Review.Current vascular pharmacology · 2025Review
- Targeting NADPH Oxidase as an Approach for Diabetic Bladder Dysfunction.Antioxidants (Basel, Switzerland) · 2024Review
- Specific NOX4 Inhibition Preserves Mitochondrial Function and Dampens Kidney Dysfunction Following Ischemia-Reperfusion-Induced Kidney Injury.Antioxidants (Basel, Switzerland) · 2024Article
- Redox Regulation of Immunometabolism in Microglia Underpinning Diabetic Retinopathy.Antioxidants (Basel, Switzerland) · 2024Review
- Reactive oxygen species in biological systems: Pathways, associated diseases, and potential inhibitors-A review.Food science & nutrition · 2024Review
- Interplay between energy metabolism and NADPH oxidase-mediated pathophysiology in cardiovascular diseases.Frontiers in pharmacology · 2024Review
- Food Polyphenols as Preventive Medicine.Antioxidants (Basel, Switzerland) · 2023Review
- NADPH Oxidases: From Molecular Mechanisms to Current Inhibitors.Journal of medicinal chemistry · 2023Review
- Anti-oxidant effect of nitrite in the pancreatic islets of type 2 diabetic male rats.Iranian journal of basic medical sciences · 2023Article
- Oxidative Stress and Its Relation to Lower Urinary Tract Symptoms.International neurourology journal · 2022Article
- NADPH Oxidases in Aortic Aneurysms.Antioxidants (Basel, Switzerland) · 2022Review
- Dapsone, More than an Effective Neuro and Cytoprotective Drug.Current neuropharmacology · 2022Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has been proposed that pancreatic beta-cell dysfunction in type 2 diabetes is promoted by oxidative stress caused by NADPH oxidase (Nox) over-activity. The aim of the present study was to evaluate the efficacy of novel Nox inhibitors as protective agents against cytokine- or high glucose + palmitate-induced human beta-cell death. The Nox2 protein was present mainly in the cytoplasm and was induced by cytokines. Nox4 protein immunoreactivity, with some nuclear accumulation, was observed in human islet cells, and was not affected by islet culture in the presence of cytokines or high glucose + palmitate. Nox inhibitors with partial or no isoform selectivity (DPI, dapsone, GLX351322, and GLX481372) all reduced ROS production of human islet cells exposed to high glucose + palmitate. This was paralleled by improved viability and reduced caspase 3 activation. The Nox1 selective inhibitor ML171 failed to reduce human islet cell death in response to both cytokines and high glucose + palmitate. The selective Nox2 inhibitor Phox-I2 also failed to protect against cytokines, but protected partially against high glucose + palmitate-induced cellular death. The highly selective Nox4 inhibitor GLX7013114 protected islet cells against both cytokines and high glucose + palmitate. However, as no osmotic control for high glucose was used, we cannot exclude the possibility that the high glucose effect was due to osmosis. It is concluded that Nox4 may participate in stress-induced islet cell death in human islets in vitro. We propose that Nox4 mediates pro-apoptotic effects in intact islets under stressful conditions and that selective Nox4-inhibition may be a therapeutic strategy in type 2 diabetes.
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