ArticleJournal of neurotrauma2017
Striatal Mitochondrial Disruption following Severe Traumatic Brain Injury.
Article in Journal of neurotrauma, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Diagnostic and Predictive Value of Circulating and Exosomal microRNAs in Ferroptosis-Associated Neurological Conditions: A Systematic Review and Meta-analysis.Molecular neurobiology · 2026Pooled it
- Mitochondrial homeostasis imbalance-triggered PANoptosis in traumatic brain and spinal cord injury: from mechanism to therapeutic strategies.Redox biology · 2026Review
- 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
- miRNAs involved in the regulation of exercise fatigue.Frontiers in physiology · 2025Review
- The Ambivalent Role of miRNA-21 in Trauma and Acute Organ Injury.International journal of molecular sciences · 2024Review
- Metabolic Diaschisis in Mild Traumatic Brain Injury.Journal of neurotrauma · 2024Article
- Mitochondrial Dysfunction and Apoptosis in Brain Microvascular Endothelial Cells Following Blast Traumatic Brain Injury.Cellular and molecular neurobiology · 2023Article
- Pathogenesis of miR-155 on nonmodifiable and modifiable risk factors in Alzheimer's disease.Alzheimer's research & therapy · 2023Review
- MiR-155: An Important Regulator of Neuroinflammation.International journal of molecular sciences · 2021Review
- Tannic Acid Provides Neuroprotective Effects Against Traumatic Brain Injury Through the PGC-1α/Nrf2/HO-1 Pathway.Molecular neurobiology · 2020Article
- Penetrating Ballistic-Like Brain Injury Leads to MicroRNA Dysregulation, BACE1 Upregulation, and Amyloid Precursor Protein Loss in Lesioned Rat Brain Tissues.Frontiers in neuroscience · 2020Article
- Proteomic Analysis and Biochemical Correlates of Mitochondrial Dysfunction after Low-Intensity Primary Blast Exposure.Journal of neurotrauma · 2019Article
- Inhibition of miR-155 Limits Neuroinflammation and Improves Functional Recovery After Experimental Traumatic Brain Injury in Mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019Article
- Lithium Improves Dopamine Neurotransmission and Increases Dopaminergic Protein Abundance in the Striatum after Traumatic Brain Injury.Journal of neurotrauma · 2018Article
- Neuroprotective effects of pifithrin-α against traumatic brain injury in the striatum through suppression of neuroinflammation, oxidative stress, autophagy, and apoptosis.Scientific reports · 2018Article
- The NADPH oxidase NOX2 mediates loss of parvalbumin interneurons in traumatic brain injury: human autoptic immunohistochemical evidence.Scientific reports · 2017Article
- Disrupted mitochondrial genes and inflammation following stroke.Life sciences · 2016Article
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Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Traumatic brain injury (TBI) results in oxidative stress and calcium dysregulation in mitochondria. However, little work has examined perturbations of mitochondrial homeostasis in peri-injury tissue. We examined mitochondrial homeostasis after a unilateral controlled cortical impact over the sensorimotor cortex in adult male rats. There was a significant reduction in peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) messenger RNA (mRNA) at post-injury days 3 and 6 and a transient reduction in mitochondrial DNA copy number at 3 days post-injury that recovered by 6 days in the ipsi-injury striatum. In ipsilateral cortex, PGC-1α mRNA was reduced only at 6 days post-injury. Additionally, expression of mitochondrial-encoded mRNAs, cytochrome c oxidase subunit 1 and NADH dehydrogenase subunit 1, was decreased at 3 and 6 days post-injury in ipsilesional striatum and at 6 days post-injury in ipsilesional cortex. There was no observable decrease in nuclear-encoded mRNAs mitochondrial transcription factor A or NADH dehydrogenase (ubiquinone) Fe-S protein 1. We detected an acute increase in superoxide dismutase 2 mRNA expression, as well as an induction of microRNA (miR)-21 and miR-155, which have been previously demonstrated to disrupt mitochondrial homeostasis. Behaviorally, rats with TBI exhibited marked error rates in contrainjury forelimb performance on the ladder test. These findings reveal that there may be differential susceptibilities of various peri-injury brain structures to mitochondrial dysfunction and associated behavioral deficits, and that molecular pathways demonstrated to interfere with mitochondrial homeostasis and function are activated subacutely post-TBI.
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Registered trials
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