ArticleNeurochemistry international2022
Antioxidant therapies in traumatic brain injury.
Article in Neurochemistry international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.
- Ginkgo biloba as a Promising Candidate for Traumatic Brain Injury: Insights From Preclinical and Clinical Studies.Chemistry & biodiversity · 2026Pooled it
- Ischemic Stroke and Traumatic Brain Injury: Epidemiology, Molecular Pathways, and Emerging Therapies.MedComm · 2026Review
- The effects of gamma glutamyl cysteinyl ethyl ester in traumatically brain injured rats post incident: insight into the role of glutathione elevation in oxidative stress.Frontiers in neuroscience · 2026Article
- Injectable reactive oxygen and nitrogen species-scavenging hydrogels for repairing traumatic brain injury.Materials today. Bio · 2025Article
- Sexually Dimorphic Responses Reveal Multifaceted Benefits of Glibenclamide in Traumatic Brain Injury.Journal of neurotrauma · 2025Article
- Exo70 Protects Against Memory and Synaptic Impairments Following Mild Traumatic Brain Injury.Antioxidants (Basel, Switzerland) · 2025Article
- Applications of Hydrogels in Emergency Therapy.Gels (Basel, Switzerland) · 2025Review
- Gallic acid alleviates ferroptosis by negatively regulating APOC3 and improves nerve function deficit caused by traumatic brain injury.Scientific reports · 2025Article
- Olfactory mucosa-mesenchymal stem cells with overexpressed Nrf2 modulate angiogenesis and exert anti-inflammation effect in an in vitro traumatic brain injury model.European journal of medical research · 2025Article
- The role of reactive oxygen species in the regulation of the blood-brain barrier.Tissue barriers · 2025Review
- Implications and pathophysiology of neuroinflammation in pediatric patients with traumatic brain injury: an updated review.Frontiers in neuroscience · 2025Review
- Mitochondrial-targeted therapies in traumatic brain injury: From bench to bedside.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Review
- The evolving pathophysiology of TBI and the advantages of temporally-guided combination therapies.Neurochemistry international · 2024Review
- Ferroptosis in radiation-induced brain injury: roles and clinical implications.Biomedical engineering online · 2024Review
- Neutrophil membrane-derived nanoparticles protect traumatic brain injury via inhibiting calcium overload and scavenging ROS.Journal of nanobiotechnology · 2024Article
- The Uncoupling Effect of 17β-Estradiol Underlies the Resilience of Female-Derived Mitochondria to Damage after Experimental TBI.Life (Basel, Switzerland) · 2024Article
- Complex Hippocampal Response to Thermal Skin Injury and Protocols with Hyperbaric Oxygen Therapy andInternational journal of molecular sciences · 2024Article
- Sestrin2 can alleviate endoplasmic reticulum stress to improve traumatic brain injury by activating AMPK/mTORC1 signaling pathway.Metabolic brain disease · 2024Review
- Mitochondria-Targeted Antioxidant Therapeutics for Traumatic Brain Injury.Antioxidants (Basel, Switzerland) · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Oxidative stress plays a crucial role in traumatic brain injury (TBI) pathogenesis. Reactive oxygen species (ROS) and reactive nitrogen species (RNS) formed in excess after TBI synergistically contribute to secondary brain damage together with lipid peroxidation products (reactive aldehydes) and inflammatory mediators. Furthermore, oxidative stress, endoplasmic reticulum stress and inflammation potentiate each other. Following TBI, excessive oxidative stress overloads the endogenous cellular antioxidant system leading to cell death. To combat oxidative stress, several antioxidant therapies were tested in preclinical animal models of TBI. These include free radical scavengers, activators of antioxidant systems, Inhibitors of free radical generating enzymes and antioxidant enzymes. Many of these therapies showed promising outcomes including reduced edema, blood-brain barrier (BBB) protection, smaller contusion volume, and less inflammation. In addition, many antioxidant therapies also promoted better sensory, motor, and cognitive functional recovery after TBI. Overall, preventing oxidative stress is a viable therapeutic option to minimize the secondary damage and to improve the quality of life after TBI.
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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.