ReviewAntioxidants & redox signaling2013
Which NADPH oxidase isoform is relevant for ischemic stroke? The case for nox 2.
Review in Antioxidants & redox signaling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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Who cites it
66 citing papers in PubMed, 123 citations in OpenAlex.
- Review
- The Role of Oxidative Stress-Induced Senescence in the Pathogenesis of Preeclampsia.Antioxidants (Basel, Switzerland) · 2025Review
- Blood-brain barrier repair: potential and challenges of stem cells and exosomes in stroke treatment.Frontiers in cellular neuroscience · 2025Review
- Features of thromboelastogram in populations exposed to or transferring from high altitude.Heliyon · 2024Article
- A network pharmacology approach to decipher the mechanism of total flavonoids from Dracocephalum Moldavica L. in the treatment of cardiovascular diseases.BMC complementary medicine and therapies · 2024Article
- Reactive oxygen species (ROS)-responsive biomaterials for treating myocardial ischemia-reperfusion injury.Frontiers in bioengineering and biotechnology · 2024Review
- Inhibition of angiotensin II type 1 receptor reduces oxidative stress damage to the intestinal barrier in severe acute pancreatitis.The Kaohsiung journal of medical sciences · 2023Article
- Fasudil mediates neuroprotection in ischemia/reperfusion by modulating the ROCK-PPARα-NOX axis.Acta cirurgica brasileira · 2023Article
- Neonatal asphyxia as an inflammatory disease: Reactive oxygen species and cytokines.Frontiers in pediatrics · 2023Review
- Edaravone dexborneol protects cerebral ischemia reperfusion injury through activating Nrf2/HO-1 signaling pathway in mice.Fundamental & clinical pharmacology · 2022Article
- NOX2-mediated reactive oxygen species are double-edged swords in focal cerebral ischemia in mice.Journal of neuroinflammation · 2022Article
- Yin and Yang of NADPH Oxidases in Myocardial Ischemia-Reperfusion.Antioxidants (Basel, Switzerland) · 2022Review
- Dehydroepiandrosterone, Cancer, and Aging.Aging and disease · 2022Review
- Identification of the NADPH Oxidase (Nox) Subtype and the Source of Superoxide Production in the Micturition Centre.Biology · 2022Article
- The Role of Oxidative Stress in Acute Ischemic Stroke-Related Thrombosis.Oxidative medicine and cellular longevity · 2022Review
- Post Stroke Safinamide Treatment Attenuates Neurological Damage by Modulating Autophagy and Apoptosis in Experimental Model of Stroke in Rats.Molecular neurobiology · 2021Article
- NADPH debt drives redox bankruptcy: SLC7A11/xCT-mediated cystine uptake as a double-edged sword in cellular redox regulation.Genes & diseases · 2021Review
- Therapeutic hypothermia augments the restorative effects of PKC-β and Nox2 inhibition on an in vitro model of human blood-brain barrier.Metabolic brain disease · 2021Article
- Article
- Role of Oxidative Stress in Reperfusion following Myocardial Ischemia and Its Treatments.Oxidative medicine and cellular longevity · 2021Review
6 more citing papers are in PubMed but not listed here.
Corrections and comments
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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
unlabelledSignificance and Recent Advances: Ischemic stroke is the leading cause of disability and third in mortality in industrialized nations. Immediate restoration of cerebral blood flow is crucial to salvage brain tissue, but only few patients are eligible for recanalization therapy. Thus, the need for alternative neuroprotective strategies is huge, and antioxidant interventions have long been studied in this context. Reactive oxygen species (ROS) physiologically serve as signaling molecules, but excessive amounts of ROS, as generated during ischemia/reperfusion (I/R), contribute to tissue injury. CRITICAL ISSUES: Nevertheless and despite a strong rational of ROS being a pharmacological target, all antioxidant interventions failed to improve functional outcome in human clinical trials. Antioxidants may interfere with physiological functions of ROS or do not reach the crucial target structures of ROS-induced injury effectively. FUTURE DIRECTIONS: Thus, a potentially more promising approach is the inhibition of the source of disease-promoting ROS. Within recent years, NADPH oxidases (Nox) of the Nox family have been identified as mediators of neuronal pathology. As, however, several Nox homologs are expressed in neuronal tissue, and as many of the pharmacological inhibitors employed are rather unspecific, the concept of Nox as mediators of brain damage is far from being settled. In this review, we will discuss the contribution of Nox homologs to I/R injury at large as well as to neuronal damage in particular. We will illustrate that the current data provide evidence for Nox2 as the most important NADPH oxidase mediating cerebral injury.
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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.