ReviewAntioxidants & redox signaling2015
Evolution of NADPH Oxidase Inhibitors: Selectivity and Mechanisms for Target Engagement.
Review in Antioxidants & redox signaling, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 296 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
296 citing papers in PubMed, 503 citations in OpenAlex.
- NADPH oxidases in immunometabolism and disease pathology: mechanistic networks, pollutant triggers, and therapeutic frontiers.Cellular & molecular immunology · 2026Review
- Solvent-driven modulation of phenolic composition and biofunctional activities of three Mentha aquatica formulations: integrated in vitro and in silico insights.Bioresources and bioprocessing · 2026Article
- Astrocytic Redox Homeostasis as a Metabolic Modulator of DNA Damage and Repair in the Ischemic Penumbra.Cells · 2026Review
- Hemostasis-Sparing Antiplatelet Therapy: Current Concepts and Emerging Targets in Arterial Thrombosis.Biomolecules & therapeutics · 2026Review
- Extracellular Redox Balance as a Determinant of Immune Regulation and Tissue Inflammation.Antioxidants (Basel, Switzerland) · 2026Review
- Pathophysiology of reactive oxygen species (ROS).Archives of toxicology · 2026Review
- Lipopeptides fromBiotech (Basel (Switzerland)) · 2026Article
- High-Altitude Hypoxia Injury: Systemic Mechanisms and Intervention Strategies on Immune and Inflammatory Responses.Antioxidants (Basel, Switzerland) · 2025Review
- Beyond Radical Scavengers: Focus on NADPH Oxidases (NOX) Inhibitors as New Agents for Antioxidant Therapy in Alzheimer's Disease.Antioxidants (Basel, Switzerland) · 2025Review
- Oxidized phosphatidylcholines activate NOX1-mediated oxidative stress response and shift glucose metabolism in cardiac cells.American journal of physiology. Cell physiology · 2025Article
- Frequency-Dependent Mechanism of 24-Hydroxycholesterol-Mediated Modulation of Neurotransmitter Release at the Mouse Neuromuscular Junction: The Role of Reactive Oxygen Species.Neurochemical research · 2025Article
- Aerobic Exercise Delays Age-Related Sarcopenia in Mice via Alleviating Imbalance in Mitochondrial Quality Control.Metabolites · 2025Article
- Enhancing Selectivity and Potency of SJournal of medicinal chemistry · 2025Article
- Oxidative Stress and Complement Activation in Aqueous Cells and Vitreous from Patient with Vitreoretinal Diseases: Comparison Between Diabetic ERM and PDR.Antioxidants (Basel, Switzerland) · 2025Article
- Ginsenoside Rg5 modulates the TLR4 and BCL-2 pathways by inhibiting NOX1, thereby alleviating inflammation, apoptosis and pyroptosis in hyperuricemia nephropathy.Journal of ginseng research · 2025Article
- Article
- Overexpression of adipose tissue ERα enhances PVAT anticontractility via NOX4-derived HAmerican journal of physiology. Heart and circulatory physiology · 2025Article
- NOX Family: Regulators of Reactive Oxygen Species Balance in Tumor Cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Review
- Fatty acid synthase (FASN) inhibition cooperates with BH3 mimetic drugs to overcome resistance to mitochondrial apoptosis in pancreatic cancer.Neoplasia (New York, N.Y.) · 2025Article
- Generation of cellular reactive oxygen and nitrogen species by exposure to ultraviolet radiation.Biophysical reviews · 2025Review
236 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
significanceOxidative stress, an excess of reactive oxygen species (ROS) production versus consumption, may be involved in the pathogenesis of different diseases. The only known enzymes solely dedicated to ROS generation are nicotinamide adenine dinucleotide phosphate (NADPH) oxidases with their catalytic subunits (NOX). After the clinical failure of most antioxidant trials, NOX inhibitors are the most promising therapeutic option for diseases associated with oxidative stress. RECENT ADVANCES: Historical NADPH oxidase inhibitors, apocynin and diphenylene iodonium, are un-specific and not isoform selective. Novel NOX inhibitors stemming from rational drug discovery approaches, for example, GKT137831, ML171, and VAS2870, show improved specificity for NADPH oxidases and moderate NOX isoform selectivity. Along with NOX2 docking sequence (NOX2ds)-tat, a peptide-based inhibitor, the use of these novel small molecules in animal models has provided preliminary in vivo evidence for a pathophysiological role of specific NOX isoforms. CRITICAL ISSUES: Here, we discuss whether novel NOX inhibitors enable reliable validation of NOX isoforms' pathological roles and whether this knowledge supports translation into pharmacological applications. Modern NOX inhibitors have increased the evidence for pathophysiological roles of NADPH oxidases. However, in comparison to knockout mouse models, NOX inhibitors have limited isoform selectivity. Thus, their use does not enable clear statements on the involvement of individual NOX isoforms in a given disease. FUTURE DIRECTIONS: The development of isoform-selective NOX inhibitors and biologicals will enable reliable validation of specific NOX isoforms in disease models other than the mouse. Finally, GKT137831, the first NOX inhibitor in clinical development, is poised to provide proof of principle for the clinical potential of NOX inhibition.
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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.