ArticleInternational journal of molecular sciences2021
Etifoxine Restores Mitochondrial Oxidative Phosphorylation and Improves Cognitive Recovery Following Traumatic Brain Injury.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- Mitochondrial dysfunction in the spinal cord contributes to peripheral hypersensitivity in a nitroglycerin-induced migraine model.Journal of translational medicine · 2026Article
- Simvastatin-induced neuroprotective effect after brain injury is mediated by mitochondrial protection through modulation of the 18 kDa translocator protein.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Diffuse traumatic brain injury in mice is associated with a transient mismatch of cerebral blood flow and energy metabolism.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026Article
- Refining seizure foci localization: the potential of TSPO-PET.Acta epileptologica · 2025Review
- Vinpocetine Ameliorates Neuronal Injury After Cold-Induced Traumatic Brain Injury in Mice.Molecular neurobiology · 2025Article
- Mitochondrial DNA leakage: underlying mechanisms and therapeutic implications in neurological disorders.Journal of neuroinflammation · 2025Review
- The link between spreading depolarization and innate immunity in the central nervous system.The journal of headache and pain · 2025Review
- From imaging to intervention: emerging potential of PET biomarkers to shape therapeutic strategies for TBI-induced neurodegeneration.Frontiers in neurology · 2025Review
- Is it possible to prevent excessive synaptic pruning in schizophrenia? Possibilities and limitations.Frontiers in synaptic neuroscience · 2025Review
- The evolving pathophysiology of TBI and the advantages of temporally-guided combination therapies.Neurochemistry international · 2024Review
- Review
- From spreading depolarization to blood-brain barrier dysfunction: navigating traumatic brain injury for novel diagnosis and therapy.Nature reviews. Neurology · 2024Review
- Mitophagy in intracerebral hemorrhage: a new target for therapeutic intervention.Neural regeneration research · 2024Review
- Hyperbaric Oxygen Therapy Alleviates Memory and Motor Impairments Following Traumatic Brain Injury via the Modulation of Mitochondrial-Dysfunction-Induced Neuronal Apoptosis in Rats.Antioxidants (Basel, Switzerland) · 2023Article
- HBO treatment enhances motor function and modulates pain development after sciatic nerve injury via protection the mitochondrial function.Journal of translational medicine · 2023Article
- Traumatic Brain Injury Alters Cerebral Concentrations and Redox States of Coenzymes QAntioxidants (Basel, Switzerland) · 2023Article
- Translocator protein in the rise and fall of central nervous system neurons.Frontiers in cellular neuroscience · 2023Review
- The Role of Hydrogen Sulfide Targeting Autophagy in the Pathological Processes of the Nervous System.Metabolites · 2022Review
- The role of regulatory necrosis in traumatic brain injury.Frontiers in molecular neuroscience · 2022Review
- Dynamic management of traumatic brain injury in rat: injectable hydrogels and future directions.Frontiers in neurologyReview
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The opening of the mitochondrial permeability transition pore (mPTP) has emerged as a pivotal event following traumatic brain injury (TBI). Evidence showing the impact of the translocator protein (TSPO) over mPTP activity has prompted several studies exploring the effect of TSPO ligands, including etifoxine, on the outcome of traumatic brain injury (TBI). Mitochondrial respiration was assessed by respirometry in isolated rat brain mitochondria (RBM) by measurements of oxidative phosphorylation capacity (OXPHOS). The addition of calcium to RBM was used to induce mitochondrial injury and resulted in significant OXPHOS reduction that could be reversed by preincubation of RBM with etifoxine. Sensorimotor and cognitive functions were assessed following controlled cortical impact and compared in vehicle and etifoxine-treated animals. There was no difference between the vehicle and etifoxine groups for sensorimotor functions as assessed by rotarod. In contrast, etifoxine resulted in a significant improvement of cognitive functions expressed by faster recovery in Morris water maze testing. The present findings show a significant neuroprotective effect of etifoxine in TBI through restoration of oxidative phosphorylation capacity associated with improved behavioral and cognitive outcomes. Since etifoxine is a registered drug used in common clinical practice, implementation in a phase II study may represent a reasonable step forward.
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