ReviewCellular and molecular life sciences : CMLS2012
NADPH oxidases as therapeutic targets in ischemic stroke.
Review in Cellular and molecular life sciences : CMLS, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 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
79 citing papers in PubMed, 127 citations in OpenAlex.
- Hypoxia-inducible factor-1α: Dual roles in maintaining neuronal homeostasis and neuronal degeneration via regulation of oxidative stress, mitochondrial dynamics, and bioenergetics.Journal of physiology and biochemistry · 2026Review
- Cerebral Ischemia-Reperfusion Injury: Unraveling the Mitophagy-Oxidative Stress Axis for Neuroprotective Strategies.International journal of molecular sciences · 2026Review
- Serum Amyloid A-Dependent Inflammasome Activation and Acute Injury in a Mouse Model of Experimental Stroke.International journal of molecular sciences · 2026Article
- HIPK2 protects neurons from oxidative stress and modulates central nervous system responses following traumatic brain injury.Iranian journal of basic medical sciences · 2026Article
- Ischemic stroke neuroprotection revisited: translational barriers and a phase-resolved, biomarker-anchored framework.Archives of pharmacal research · 2026Review
- Identification of key genes associated with oxidative stress in ischemic stroke via bioinformatics integrated analysis.BMC neuroscience · 2025Article
- Neuroinflammation and acute ischemic stroke: impact on translational research and clinical care.Frontiers in surgery · 2025Review
- Transcriptome Sequencing-Based Screening of Key Melatonin-Related Genes in Ischemic Stroke.International journal of molecular sciences · 2024Article
- Article
- Neuroprotective Effects of Phenolic Antioxidant Tert-butylhydroquinone (tBHQ) in Brain Diseases.Molecular neurobiology · 2023Review
- A Comparative Analysis of Neuroprotective Properties of Taxifolin and Its Water-Soluble Form in Ischemia of Cerebral Cortical Cells of the Mouse.International journal of molecular sciences · 2023Article
- The Role of Potential Oxidative Biomarkers in the Prognosis of Acute Ischemic Stroke and the Exploration of Antioxidants as Possible Preventive and Treatment Options.International journal of molecular sciences · 2023Review
- Neutrophil Extracellular Traps in Cerebral Ischemia/Reperfusion Injury: Friend and Foe.Current neuropharmacology · 2023Review
- Atorvastatin alleviates oxidative damage by activating the nuclear factor erythroid 2-related factor 2 pathway after brain ischemia in mice.Annals of translational medicine · 2022Article
- Edaravone dexborneol protects cerebral ischemia reperfusion injury through activating Nrf2/HO-1 signaling pathway in mice.Fundamental & clinical pharmacology · 2022Article
- Identification of changed proteins by retinoic acid in cerebral ischemic damage: a proteomic study.The Journal of veterinary medical science · 2022Article
- Ubiquitin-specific protease 7 regulates myocardial ischemia/reperfusion injury by stabilizing Keap1.Cell death discovery · 2022Article
- Effects of ischemic postconditioning and long non-coding RNAs in ischemic stroke.Bioengineered · 2022Review
- (±)-5-bromo-2-(5-fluoro-1-hydroxyamyl) Benzoate Protects Against Oxidative Stress Injury in PC12 Cells Exposed to HFrontiers in pharmacology · 2022Article
- The Role of Oxidative Stress in Acute Ischemic Stroke-Related Thrombosis.Oxidative medicine and cellular longevity · 2022Review
19 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reactive oxygen species (ROS) act physiologically as signaling molecules. In pathological conditions, such as ischemic stroke, ROS are released in excessive amounts and upon reperfusion exceed the body's antioxidant detoxifying capacity. This process leads to brain tissue damage during reoxygenation. Consequently, antioxidant strategies have long been suggested as a therapy for experimental stroke, but clinical trials have not yet been able to promote the translation of this concept into patient treatment regimens. As an evolution of this concept, recent studies have targeted the sources of ROS generation-rather than ROS themselves. In this context, NADPH oxidases have been identified as important generators of ROS in the cerebral vasculature under both physiological conditions in general and during ischemia/reoxygenation in particular. Inhibition of NADPH oxidases or genetic deletion of certain NADPH oxidase isoforms has been found to considerably reduce ischemic injury in experimental stroke. This review focuses on recent advances in the understanding of NADPH oxidase-mediated tissue injury in the cerebral vasculature, particularly at the level of the blood-brain barrier, and highlights promising inhibitory strategies that target the NADPH oxidases.
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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.