ArticlePloS one2013
K(ATP) channel opener diazoxide prevents neurodegeneration: a new mechanism of action via antioxidative pathway activation.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 27 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
27 citing papers in PubMed, 47 citations in OpenAlex.
- Unlocking Neuroprotection: Potassium Channel Openers in Alzheimer's Disease.Current Alzheimer research · 2026Review
- Glial Ion Channels in Myelin Pathophysiology: Insights from Leukodystrophies.Life (Basel, Switzerland) · 2025Review
- Network medicine informed multiomics integration identifies drug targets and repurposable medicines for Amyotrophic Lateral Sclerosis.NPJ systems biology and applications · 2024Article
- Gliclazide Ameliorates Neuronal Injury by Attenuating Oxidative Stress in D-gal-Induced Senescent Cells and Aging Mice.Molecular neurobiology · 2024Article
- Network medicine informed multi-omics integration identifies drug targets and repurposable medicines for Amyotrophic Lateral Sclerosis.bioRxiv : the preprint server for biology · 2024Article
- Timed sulfonylurea modulation improves locomotor and sensory dysfunction following spinal cord injury.Frontiers in pharmacology · 2024Article
- Hyperinsulinism May Be Underreported in Hypoglycemic Patients with Phosphomannomutase 2 DeficiencyJournal of clinical research in pediatric endocrinology · 2022Article
- Discovery of Therapeutics Targeting Oxidative Stress in Autosomal Recessive Cerebellar Ataxia: A Systematic Review.Pharmaceuticals (Basel, Switzerland) · 2022Review
- The 40-Hz White Light-Emitting Diode (LED) Improves the Structure-Function of the Brain Mitochondrial KATP Channel and Respiratory Chain Activities in Amyloid Beta Toxicity.Molecular neurobiology · 2022Article
- Somatostatin-evoked Aβ catabolism in the brain: Mechanistic involvement of α-endosulfine-KMolecular psychiatry · 2022Article
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- Review
- Hypoglycemia in CDG patients due to PMM2 mutations: Follow up on hyperinsulinemic patients.JIMD reports · 2020Article
- Article
- Ions, the Movement of Water and the Apoptotic Volume Decrease.Frontiers in cell and developmental biology · 2020Review
- KMolecular neurobiology · 2018Article
- Health Risks of Hypovitaminosis D: A Review of New Molecular Insights.International journal of molecular sciences · 2018Review
- Hypoglycemia in the preterm neonate: etiopathogenesis, diagnosis, management and long-term outcomes.Translational pediatrics · 2017Review
- Effects of diazoxide in experimental acute necrotizing pancreatitis.Clinics (Sao Paulo, Brazil) · 2017Article
- Molecular Bases of Brain Preconditioning.Frontiers in neuroscience · 2017Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pharmacological modulation of ATP-sensitive potassium channels has become a promising new therapeutic approach for the treatment of neurodegenerative diseases due to their role in mitochondrial and cellular protection. For instance, diazoxide, a well-known ATP-sensitive potassium channel activator with high affinity for mitochondrial component of the channel has been proved to be effective in animal models for different diseases such as Alzheimer's disease, stroke or multiple sclerosis. Here, we analyzed the ability of diazoxide for protecting neurons front different neurotoxic insults in vitro and ex vivo. Results showed that diazoxide effectively protects NSC-34 motoneurons from glutamatergic, oxidative and inflammatory damage. Moreover, diazoxide decreased neuronal death in organotypic hippocampal slice cultures after exicitotoxicity and preserved myelin sheath in organotypic cerebellar cultures exposed to pro-inflammatory demyelinating damage. In addition, we demonstrated that one of the mechanisms of actions implied in the neuroprotective role of diazoxide is mediated by the activation of Nrf2 expression and nuclear translocation. Nrf2 expression was increased in NSC-34 neurons in vitro as well as in the spinal cord of experimental autoimmune encephalomyelitis animals orally administered with diazoxide. Thus, diazoxide is a neuroprotective agent against oxidative stress-induced damage and cellular dysfunction that can be beneficial for diseases such as multiple sclerosis.
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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.