ArticleAntioxidants & redox signaling2015
NADPH oxidase-2: linking glucose, acidosis, and excitotoxicity in stroke.
Article 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 30 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
30 citing papers in PubMed, 54 citations in OpenAlex.
- Hypoxia-inducible factor-1: A new neuroprotective agent for the treatment of hyperglycemia after stroke.Neural regeneration research · 2026Article
- 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
- Transcriptional and neuroprotective effects of hexokinase-2 inhibitors administered after stroke.Journal of neuroinflammation · 2025Article
- NOX2 in Alzheimer's and Parkinson's disease.Redox biology · 2024Review
- NOX-induced oxidative stress is a primary trigger of major neurodegenerative disorders.Progress in neurobiology · 2023Review
- Crocetin antagonizes parthanatos in ischemic stroke via inhibiting NOX2 and preserving mitochondrial hexokinase-I.Cell death & disease · 2023Article
- CircDLGAP4 overexpression relieves oxygen-glucose deprivation-induced neuronal injury by elevating NEGR1 through sponging miR-503-3p.Journal of molecular histology · 2022Article
- Treatment of Cerebral Ischemia Through NMDA Receptors: Metabotropic Signaling and Future Directions.Frontiers in pharmacology · 2022Review
- Aβ initiates brain hypometabolism, network dysfunction and behavioral abnormalities via NOX2-induced oxidative stress in mice.Communications biology · 2021Article
- Genetically encoded cell-death indicators (GEDI) to detect an early irreversible commitment to neurodegeneration.Nature communications · 2021Article
- The secretome of endothelial progenitor cells: a potential therapeutic strategy for ischemic stroke.Neural regeneration research · 2021Article
- The Role of NADPH Oxidase in Neuronal Death and Neurogenesis after Acute Neurological Disorders.Antioxidants (Basel, Switzerland) · 2021Review
- Quercetin Disaggregates Prion Fibrils and Decreases Fibril-Induced Cytotoxicity and Oxidative Stress.Pharmaceutics · 2020Article
- Rac1 relieves neuronal injury induced by oxygenglucose deprivation and re-oxygenation via regulation of mitochondrial biogenesis and function.Neural regeneration research · 2020Article
- Nicotinamide adenine dinucleotide phosphate oxidase activation and neuronal death after ischemic stroke.Neural regeneration research · 2019Review
- Excitotoxic superoxide production and neuronal death require both ionotropic and non-ionotropic NMDA receptor signaling.Scientific reports · 2018Article
- Scutellarin protects oxygen/glucose-deprived astrocytes and reduces focal cerebral ischemic injury.Neural regeneration research · 2018Article
- Acidosis mediates recurrent hypoglycemia-induced increase in ischemic brain injury in treated diabetic rats.Neuropharmacology · 2018Article
- Neuronal Cell Death.Physiological reviews · 2018Review
- Acid sphingomyelinase promotes mitochondrial dysfunction due to glutamate-induced regulated necrosis.Journal of lipid research · 2018Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
significanceNeuronal superoxide production contributes to cell death in both glutamate excitotoxicity and brain ischemia (stroke). NADPH oxidase-2 (NOX2) is the major source of neuronal superoxide production in these settings, and regulation of NOX2 activity can thereby influence outcome in stroke. RECENT ADVANCES: Reduced NOX2 activity can rescue cells from oxidative stress and cell death that otherwise occur in excitotoxicity and ischemia. NOX2 activity is regulated by several factors previously shown to affect outcome in stroke, including glucose availability, intracellular pH, protein kinase ζ/δ, casein kinase 2, phosphoinositide-3-kinase, Rac1/2, and phospholipase A2. The newly identified functions of these factors as regulators of NOX2 activity suggest alternative mechanisms for their effects on ischemic brain injury. CRITICAL ISSUES: Key aspects of these regulatory influences remain unresolved, including the mechanisms by which rac1 and phospholipase activities are coupled to N-methyl-D-aspartate (NMDA) receptors, and whether superoxide production by NOX2 triggers subsequent superoxide production by mitochondria. FUTURE DIRECTIONS: It will be important to establish whether interventions targeting the signaling pathways linking NMDA receptors to NOX2 in brain ischemia can provide a greater neuroprotective efficacy or a longer time window to treatment than provided by NMDA receptor blockade alone. It will likewise be important to determine whether dissociating superoxide production from the other signaling events initiated by NMDA receptors can mitigate the deleterious effects of NMDA receptor blockade.
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Registered trials
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.