ReviewCellular and molecular life sciences : CMLS2012
Targeting NOX enzymes in the central nervous system: therapeutic opportunities.
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 39 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
39 citing papers in PubMed, 75 citations in OpenAlex.
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- Molecular Targets for Intracranial Aneurysm Treatment.International journal of molecular sciences · 2025Review
- Human endogenous retrovirus W family envelope protein (ERVWE1) regulates macroautophagy activation and micromitophagy inhibition via NOXA1 in schizophrenia.Virologica Sinica · 2025Article
- Apocynin Prevents Cigarette Smoke-Induced Anxiety-Like Behavior and Preserves Microglial Profiles in Male Mice.Antioxidants (Basel, Switzerland) · 2024Article
- Nox, Nox, Are You There? The Role of NADPH Oxidases in the Peripheral Nervous System.Antioxidants & redox signaling · 2022Review
- NADPH Oxidases in Pain Processing.Antioxidants (Basel, Switzerland) · 2022Review
- Mechanisms Underlying Curcumin-Induced Neuroprotection in Cerebral Ischemia.Frontiers in pharmacology · 2022Review
- Serum NOX1 and Raftlin as New Potential Biomarkers of Interest in Schizophrenia: A Preliminary Study.Neuropsychiatric disease and treatment · 2022Article
- N-3 PUFA Prevent Oxidative Stress in a Rat Model of Beta-Amyloid-Induced Toxicity.Pharmaceuticals (Basel, Switzerland) · 2021Article
- NOX1/NADPH Oxidase Promotes Synaptic Facilitation Induced by Repeated DThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Inflammation and Oxidative Stress: Potential Targets for Improving Prognosis After Subarachnoid Hemorrhage.Frontiers in cellular neuroscience · 2021Review
- MsrA Suppresses Inflammatory Activation of Microglia and Oxidative Stress to Prevent Demyelination via Inhibition of the NOX2-MAPKs/NF-κB Signaling Pathway.Drug design, development and therapy · 2020Article
- The Link of the Prion Protein with CaInternational journal of molecular sciences · 2019Review
- Sweet Stress: Coping With Vascular Dysfunction in Diabetic Retinopathy.Frontiers in physiology · 2018Review
- Redox-based therapeutics in neurodegenerative disease.British journal of pharmacology · 2017Review
- Long-Term Effects of Maternal Deprivation on Redox Regulation in Rat Brain: Involvement of NADPH Oxidase.Oxidative medicine and cellular longevity · 2017Article
- Actin filaments-A target for redox regulation.Cytoskeleton (Hoboken, N.J.) · 2016Review
- Salidroside alleviates oxidative stress in the liver with non- alcoholic steatohepatitis in rats.BMC pharmacology & toxicology · 2016Article
- [Salidroside protects PC12 cells from HNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Among the pathogenic mechanisms underlying central nervous system (CNS) diseases, oxidative stress is almost invariably described. For this reason, numerous attempts have been made to decrease reactive oxygen species (ROS) with the administration of antioxidants as potential therapies for CNS disorders. However, such treatments have always failed in clinical trials. Targeting specific sources of reactive oxygen species in the CNS (e.g. NOX enzymes) represents an alternative promising option. Indeed, NOX enzymes are major generators of ROS, which regulate progression of CNS disorders as diverse as amyotrophic lateral sclerosis, schizophrenia, Alzheimer disease, Parkinson disease, and stroke. On the other hand, in autoimmune demyelinating diseases, ROS generated by NOX enzymes are protective, presumably by dampening the specific immune response. In this review, we discuss the possibility of developing therapeutics targeting NADPH oxidase (NOX) enzymes for the treatment of different CNS pathologies. Specific compounds able to modulate the activation of NOX enzymes, and the consequent production of ROS, could fill the need for disease-modifying drugs for many incurable CNS pathologies.
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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.