ReviewFrontiers in cellular neuroscience2025
Mitochondria: the hidden engines of traumatic brain injury-driven neurodegeneration.
Review in Frontiers in cellular neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Effects of lactate-based therapies on intracranial pressure and brain metabolism of patients with acute brain injury: a systematic review.Critical care (London, England) · 2026Pooled it
- Post-Translational Modifications in Traumatic Brain Injury: Decoding the Proteomic Landscape and Molecular Mechanisms of Secondary Injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- Pediatric Mild Traumatic Brain Injury and Concussion: Modern Pathophysiological Insights, Diagnostic Advances, and Active Management Protocols.Brain sciences · 2026Review
- Transcriptome and Experimental Verification Identified Candidate Biomarkers Related to Mitochondrial Metabolism in Sepsis-Associated Encephalopathy.Shock (Augusta, Ga.) · 2026Article
- Acupuncture regulates mitochondrial homeostasis in traumatic brain injury: current evidence, mechanistic hypotheses, and translational challenges.Chinese medicine · 2026Review
- Electroacupuncture Prevents TBI-Induced Synaptic Loss by Inhibiting CaMKII/Drp1-Dependent Mitochondrial Fission.Biomolecules · 2026Article
- Transglutaminase 2 Deletion Enhances Astrocyte-to-Neuron Metabolic Support and Attenuates Subacute Pathology Following Repetitive Mild Traumatic Brain Injury.bioRxiv : the preprint server for biology · 2026Article
- Traumatic Brain Injury Modulates Synuclein-Associated Transcription, Amyloid Plaque Morphology and Cognitive Performance in APPswe/PS1dE9/Blg Mice.Biomedicines · 2026Article
- Fenofibrate alleviates the brain edema after traumatic brain injury by enhancing endothelial OXPHOS.Redox biology · 2026Article
- Advances in the Core Role and Mechanisms of Mitochondrial Dysfunction in Alzheimer's Disease.Brain and behavior · 2026Review
- β-Lapachone-Induced Oxidative Stress Causes PARP-Dependent NADNeurochemical research · 2026Article
- Mitochondrial Dysfunction in Traumatic Brain Injury and Its Theranostic Implications.Biomolecules · 2026Review
- Microglia Mitochondria Support Neuronal Maturation via Metabolic and Transcriptional Reprogramming in Human 3D In Vitro Brain Model.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Mitochondrial dysfunction in neonatal brain injury: from molecular mechanisms to therapeutic interventions.Journal of translational medicine · 2026Review
- Elovanoid neuroprotection targets cell transcriptomics and proteomics to sustain synaptic integrity after brain injury.Communications biology · 2026Article
- Endoplasmic Reticulum-Mitochondrial Crosstalk in Calcium Regulation: Mechanistic Insights and Therapeutic Implications in Traumatic Brain Injury.Molecular neurobiology · 2026Review
- A single large-scale mitochondrial DNA deletion presenting as rapidly progressive dementia in a 35-year-old male.NPJ dementia · 2026Article
- Development and validation of a risk stratification tool for 28-day mortality based on D-dimer to platelet ratio in moderate-to -severe traumatic brain injury: a retrospective cohort study.Frontiers in neuroscience · 2026Article
- Synaptic Pathology in Traumatic Brain Injury and Therapeutic Insights.International journal of molecular sciences · 2025Review
- Endothelial mitochondria in the blood-brain barrier.Fluids and barriers of the CNS · 2025Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Mitochondria play a critical role in brain energy metabolism, cellular signaling, and homeostasis, making their dysfunction a key driver of secondary injury progression in traumatic brain injury (TBI). This review explores the relationship between mitochondrial bioenergetics, metabolism, oxidative stress, and neuroinflammation in the post-TBI brain. Mitochondrial dysfunction disrupts adenosine triphosphate (ATP) production, exacerbates calcium dysregulation, and generates reactive oxygen species, triggering a cascade of neuronal damage and neurodegenerative processes. Moreover, damaged mitochondria release damage-associated molecular patterns (DAMPs) such as mitochondrial DNA (mtDNA), Cytochrome C, and ATP, triggering inflammatory pathways that amplify tissue injury. We discuss the metabolic shifts that occur post-TBI, including the transition from oxidative phosphorylation to glycolysis and the consequences of metabolic inflexibility. Potential therapeutic interventions targeting mitochondrial dynamics, bioenergetic support, and inflammation modulation are explored, highlighting emerging strategies such as mitochondrial-targeted antioxidants, metabolic substrate supplementation, and pharmacological regulators of mitochondrial permeability transition pores. Understanding these mechanisms is crucial for developing novel therapeutic approaches to mitigate neurodegeneration and enhance recovery following brain trauma.
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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.