ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1998
Overexpression of SOD1 in transgenic rats protects vulnerable neurons against ischemic damage after global cerebral ischemia and reperfusion.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers.
What it found
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Who cites it
112 citing papers in PubMed, 341 citations in OpenAlex.
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- Excitotoxic neuronal death requires superoxide entry into neurons through volume-regulated anion channels.Science advances · 2025Article
- Growth Differentiation Factor-15 Knockout Mice Are Protected from Neonatal Hypoxic-Ischemic Injury in a Sex-Dependent Manner.Developmental neuroscience · 2025Article
- Effect of umbilical cord mesenchymal stem cell-derived mitochondrial transplantation on ischemia-reperfusion injury in a rat model.Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) · 2024Article
- Technical development of senescence-associated β-galactosidase staining in frozen kidney tissue of Sprague Dawley rat.Aging pathobiology and therapeutics · 2024Article
- Exploring Copper's role in stroke: progress and treatment approaches.Frontiers in pharmacology · 2024Review
- Aucubin Exerts Neuroprotection against Forebrain Ischemia and Reperfusion Injury in Gerbils through Antioxidative and Neurotrophic Effects.Antioxidants (Basel, Switzerland) · 2023Article
- Serum proteome alterations during conventional and extracorporeal resuscitation in pigs.Journal of translational medicine · 2022Article
- Mitochondrial Oxidative Stress-A Causative Factor and Therapeutic Target in Many Diseases.International journal of molecular sciences · 2021Review
- Oxidative Stress-Related Susceptibility to Aneurysm in Marfan's Syndrome.Biomedicines · 2021Review
- Brain vulnerability and viability after ischaemia.Nature reviews. Neuroscience · 2021Review
- X-Irradiation at 0.5 Gy after the forced swim test reduces forced swimming-induced immobility in mice.Journal of radiation research · 2020Article
- TNF receptor-associated factor 6 interacts with ALS-linked misfolded superoxide dismutase 1 and promotes aggregation.The Journal of biological chemistry · 2020Article
- Protein production is an early biomarker for RNA-targeted therapies.Annals of clinical and translational neurology · 2018Article
- Increased Superoxide Dismutase 2 by Allopregnanolone Ameliorates ROS-Mediated Neuronal Death in Mice with Pilocarpine-Induced Status Epilepticus.Neurochemical research · 2018Article
- Mitochondrial Dysfunction in Stroke: Implications of Stem Cell Therapy.Translational stroke research · 2018Review
- Nrf2-a Promising Therapeutic Target for Defensing Against Oxidative Stress in Stroke.Molecular neurobiology · 2017Review
- Differences in Reperfusion-Induced Mitochondrial Oxidative Stress and Cell Death Between Hippocampal CA1 and CA3 Subfields Are Due to the Mitochondrial Thioredoxin System.Antioxidants & redox signaling · 2017Article
- PretreatedChinese medical journal · 2017Article
52 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Transient global cerebral ischemia resulting from cardiac arrest is known to cause selective death in vulnerable neurons, including hippocampal CA1 pyramidal neurons. It is postulated that oxygen radicals, superoxide in particular, are involved in cell death processes. To test this hypothesis, we first used in situ imaging of superoxide radical distribution by hydroethidine oxidation in vulnerable neurons. We then generated SOD1 transgenic (Tg) rats with a five-fold increase in copper zinc superoxide dismutase activity. The Tg rats and their non-Tg wild-type littermates were subjected to 10 min of global ischemia followed by 1 and 3 d of reperfusion. Neuronal damage, as assessed by cresyl violet staining and DNA fragmentation analysis, was significantly reduced in the hippocampal CA1 region, cortex, striatum, and thalamus in SOD1 Tg rats at 3 d, as compared with the non-Tg littermates. There were no changes in the hippocampal CA3 subregion and dentate gyrus, resistant areas in both SOD1 Tg and non-Tg rats. Quantitative analysis of the damaged CA1 subregion showed marked neuroprotection against transient global cerebral ischemia in SOD1 Tg rats. These results suggest that superoxide radicals play a role in the delayed ischemic death of hippocampal CA1 neurons. Our data also indicate that SOD1 Tg rats are useful tools for studying the role of oxygen radicals in the pathogenesis of neuronal death after transient global cerebral ischemia.
Indexed as
Identifiers
9763473PMC6792858W1527017265What OpenQuestion holds
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.