ArticleNeurochemistry international2017
Time courses of post-injury mitochondrial oxidative damage and respiratory dysfunction and neuronal cytoskeletal degradation in a rat model of focal traumatic brain injury.
Article in Neurochemistry international, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 2 of them syntheses that pooled it.
What it found
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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.
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.
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Who cites it
65 citing papers in PubMed, 2 syntheses or guidelines pooled it, 89 citations in OpenAlex.
- Calpain Inhibitors as Potential Therapeutic Modulators in Neurodegenerative Diseases.Neurochemical research · 2022Pooled it
- Pre-Clinical Testing of Therapies for Traumatic Brain Injury.Journal of neurotrauma · 2018Guideline
- Ischemic Stroke and Traumatic Brain Injury: Epidemiology, Molecular Pathways, and Emerging Therapies.MedComm · 2026Review
- Lipid Metabolism in Central Nervous System Diseases: Pathological Mechanisms and Therapeutic Advances.CNS neuroscience & therapeutics · 2026Review
- Neuron-derived mitochondrial DNA (mtDNA) activates microglia via the Z-DNA binding protein 1 (ZBP1)-mediated pathway in mild traumatic brain injury.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Ceramide-rich extracellular vesicles as pathogenic biomarkers in traumatic brain injury.bioRxiv : the preprint server for biology · 2026Article
- Traumatic brain injury exacerbates mitochondrial dysfunction in APP/PS1 knock-in mice through time-dependent pathways.Experimental neurology · 2026Article
- The impact of and changes in the oxidative status in the post-injury period following nonpenetrating traumatic brain injuries.The Journal of international medical research · 2026Article
- Oxidative stress as a driver of organelle cascade damage in neurological diseases.Frontiers in aging neuroscience · 2026Review
- Remimazolam Attenuates Neurological Injury After TBI: A Potential Role of α7nAChR-Associated Mitophagy Enhancement and Pyroptosis Suppression in BV2 Cells.Drug design, development and therapy · 2026Article
- Traumatic brain injury exacerbates mitochondrial dysfunction in APP/PS1 knock-in mice through time-dependent pathways.bioRxiv : the preprint server for biology · 2025Article
- Review
- Perspectives on the interpretation of mitochondrial responses during skeletal muscle disuse-induced atrophy.The Journal of physiology · 2025Review
- Metabolic Imaging of Hyperpolarized [1-International journal of molecular sciences · 2025Article
- Remimazolam attenuated lipopolysaccharide-induced behavioral deficits and neuronal injury via activation of the Nrf2 pathway.Scientific reports · 2025Article
- Time Course of Mitochondrial Antioxidant Markers in a Preclinical Model of Severe Penetrating Traumatic Brain Injury.International journal of molecular sciences · 2025Article
- Antisecretory Factor 16 (AF16): A Promising Avenue for the Treatment of Traumatic Brain Injury-An In Vitro Model Approach.Journal of molecular neuroscience : MN · 2024Article
- Tracing the path of disruption:CNS neuroscience & therapeutics · 2024Review
- The role of mitochondrial uncoupling in the regulation of mitostasis after traumatic brain injury.Neurochemistry international · 2024Article
- Oxidative stress in the brain-lung crosstalk: cellular and molecular perspectives.Frontiers in aging neuroscience · 2024Review
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Traumatic brain injury (TBI) results in rapid reactive oxygen species (ROS) production and oxidative damage to essential brain cellular components leading to neuronal dysfunction and cell death. It is increasingly appreciated that a major player in TBI-induced oxidative damage is the reactive nitrogen species (RNS) peroxynitrite (PN) which is produced in large part in injured brain mitochondria. Once formed, PN decomposes into highly reactive free radicals that trigger membrane lipid peroxidation (LP) of polyunsaturated fatty acids (e.g. arachidonic acid) and protein nitration (3-nitrotyrosine, 3-NT) in mitochondria and other cellular membranes causing various functional impairments to mitochondrial oxidative phosphorylation and calcium (Ca
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What 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.