ReviewBritish journal of pharmacology2012
Mitochondria in traumatic brain injury and mitochondrial-targeted multipotential therapeutic strategies.
Review in British journal of pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 193 papers, 3 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
193 citing papers in PubMed, 3 syntheses or guidelines pooled it, 340 citations in OpenAlex.
- Therapeutic efficacy and safety of Xuebijing in traumatic brain injury: systematic review and meta-analysis.Frontiers in pharmacology · 2025Pooled it
- Exploring the biological basis of acupuncture treatment for traumatic brain injury: a review of evidence from animal models.Frontiers in cellular neuroscience · 2024Pooled it
- Pooled it
- Elevated levels of plasma mitochondrial DNA DAMPs are linked to clinical outcome in severely injured human subjects.Annals of surgery · 2013Trial
- Fumarate Hydratase Lactylation Exacerbates Traumatic Brain Injury Pathology via Mitochondrial Dysfunction and Neuroinflammation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Pediatric Mild Traumatic Brain Injury and Concussion: Modern Pathophysiological Insights, Diagnostic Advances, and Active Management Protocols.Brain sciences · 2026Review
- Thiol-Based Neuroprotective Copolymers Acutely Restore Redox Metabolism and Mediate Vasogenic Edema in a Mouse Model of Traumatic Brain Injury.Macromolecular bioscience · 2026Article
- Semaglutide Inhibits Neuronal Apoptosis and Improves Cognitive Function in Mice after Traumatic Brain Injury, Mainly via the Caspase-Dependent Pathway.Neurocritical care · 2026Article
- Mitochondrial Dysfunction in Traumatic Brain Injury and Its Theranostic Implications.Biomolecules · 2026Review
- Self-assembling scaffolds epigenetically reactivate and electroactively guide neuronal regeneration to restore central neural circuits.Nature communications · 2026Article
- Induction of activating transcription factor 3 (ATF3) in the cerebral cortex of a mouse model of blast-induced traumatic brain injury.Human cell · 2026Article
- Traumatic brain injury exacerbates mitochondrial dysfunction in APP/PS1 knock-in mice through time-dependent pathways.Experimental neurology · 2026Article
- Effect of Traumatic Brain Injury on Sensorimotor Gating.Biological psychiatry. Cognitive neuroscience and neuroimaging · 2026Article
- Celastrol Ameliorates Vincristine-induced Neuropathic Pain by Inhibiting Spinal Astrocyte Hyperactivation-mediated Inflammation, Oxidative Stress, and Apoptosis.Current neuropharmacology · 2026Article
- Peritumoral edema in meningiomas: a review of influencing factors, mechanisms, and management.Frontiers in oncology · 2026Review
- A Model of Traumatic Brain Injury Oligomerizes Tau in Cortical Organoids and Induces Clinically Relevant Pathologies that Synergize withJournal of neurotrauma · 2025Article
- Traumatic brain injury exacerbates mitochondrial dysfunction in APP/PS1 knock-in mice through time-dependent pathways.bioRxiv : the preprint server for biology · 2025Article
- Synaptic Pathology in Traumatic Brain Injury and Therapeutic Insights.International journal of molecular sciences · 2025Review
- Unlocking therapeutic potential in traumatic brain injury: exploring microenvironmental targets, signaling pathways and translational hurdles.Inflammopharmacology · 2025Review
- Temporal Changes in Mitochondria-Centric Excitotoxic Responses Following Severe Penetrating Traumatic Brain Injury.Biomedicines · 2025Article
133 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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Traumatic brain injury (TBI) is a major health and socioeconomic problem throughout the world. It is a complicated pathological process that consists of primary insults and a secondary insult characterized by a set of biochemical cascades. The imbalance between a higher energy demand for repair of cell damage and decreased energy production led by mitochondrial dysfunction aggravates cell damage. At the cellular level, the main cause of the secondary deleterious cascades is cell damage that is centred in the mitochondria. Excitotoxicity, Ca(2+) overload, reactive oxygen species (ROS), Bcl-2 family, caspases and apoptosis inducing factor (AIF) are the main participants in mitochondria-centred cell damage following TBI. Some preclinical and clinical results of mitochondria-targeted therapy show promise. Mitochondria- targeted multipotential therapeutic strategies offer new hope for the successful treatment of TBI and other acute brain injuries.
Indexed as
Identifiers
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.