ReviewTranslational neuroscience2015
The emerging neuroprotective role of mitochondrial uncoupling protein-2 in traumatic brain injury.
Review in Translational neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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.
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Who cites it
23 citing papers in PubMed, 34 citations in OpenAlex.
- Synaptic Mitochondrial Respiration Differs Between the Prefrontal Cortex and Hippocampus in C57Bl/6NTac Mice.Molecular neurobiology · 2026Article
- Synaptic mitochondrial respiration differs between the prefrontal cortex and hippocampus in female, but not male, mice: no effect of chronic stress history.Research square · 2025Article
- Mitochondrial Uncoupling Protein-2 Ameliorates Ischemic Stroke by Inhibiting Ferroptosis-Induced Brain Injury and Neuroinflammation.Molecular neurobiology · 2025Article
- Toxicological analysis of metabolites in ischemic stroke based on salivary metabolomics.Frontiers in molecular biosciences · 2025Article
- Dexamethasone-Enhanced Continuous Online Microdialysis for Neuromonitoring of OACS chemical neuroscience · 2023Article
- Uncoupling Proteins as Therapeutic Targets for Neurodegenerative Diseases.International journal of molecular sciences · 2022Review
- Mitochondria as the target for disease related hormonal dysregulation.Brain, behavior, & immunity - health · 2021Article
- Neuroprotective Effects of Exogenous Irisin in Kainic Acid-Induced Status Epilepticus.Frontiers in cellular neuroscience · 2021Article
- Research Progress on the Ability of Astragaloside IV to Protect the Brain Against Ischemia-Reperfusion Injury.Frontiers in neuroscience · 2021Review
- Irisin Rescues Blood-Brain Barrier Permeability following Traumatic Brain Injury and Contributes to the Neuroprotection of Exercise in Traumatic Brain Injury.Oxidative medicine and cellular longevity · 2021Article
- Mitochondrial electron transport chain: Oxidative phosphorylation, oxidant production, and methods of measurement.Redox biology · 2020Review
- Deletion of Mitochondrial Uncoupling Protein 2 Exacerbates Mitochondrial Damage in Mice Subjected to Cerebral Ischemia and Reperfusion Injury under both Normo- and Hyperglycemic Conditions.International journal of biological sciences · 2020Article
- UCP2 silencing aggravates mitochondrial dysfunction in astrocytes under septic conditions.Molecular medicine reports · 2019Article
- Mitochondrial Uncoupling: A Key Controller of Biological Processes in Physiology and Diseases.Cells · 2019Review
- Cytoprotective Effects of Dinitrosyl Iron Complexes on Viability of Human Fibroblasts and Cardiomyocytes.Frontiers in pharmacology · 2019Article
- AVE 0991 attenuates oxidative stress and neuronal apoptosis via Mas/PKA/CREB/UCP-2 pathway after subarachnoid hemorrhage in rats.Redox biology · 2019Article
- Rapamycin treatment increases hippocampal cell viability in an mTOR-independent manner during exposure to hypoxia mimetic, cobalt chloride.BMC neuroscience · 2018Article
- Mitochondrial Uncoupling Proteins: Subtle Regulators of Cellular Redox Signaling.Antioxidants & redox signaling · 2018Review
- Quantitative Proteomics After Spinal Cord Injury (SCI) in a Regenerative and a Nonregenerative Stage in the FrogMolecular & cellular proteomics : MCP · 2018Article
- Reduced brain UCP2 expression mediated by microRNA-503 contributes to increased stroke susceptibility in the high-salt fed stroke-prone spontaneously hypertensive rat.Cell death & disease · 2017Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Traumatic brain injury (TBI) is a multifaceted disease with intrinsically complex heterogeneity and remains a significant clinical challenge to manage. TBI model systems have demonstrated many mechanisms that contribute to brain parenchymal cell death, including glutamate and calcium toxicity, oxidative stress, inflammation, and mitochondrial dysfunction. Mitochondria are critically regulated by uncoupling proteins (UCP), which allow protons to leak back into the matrix and thus reduce the mitochondrial membrane potential by dissipating the proton motive force. This uncoupling of oxidative phosphorylation from adenosine triphosphate (ATP) synthesis is potentially critical for protection against cellular injury as a result of TBI and stroke. A greater understanding of the underlying mechanism or mechanisms by which uncoupling protein-2 (UCP2) functions to maintain or optimize mitochondrial function, and the conditions which precipitate the failure of these mechanisms, would inform future research and treatment strategies. We posit that UCP2-mediated function underlies the physiological response to neuronal stress associated with traumatic and ischemic injury and that clinical development of UCP2-targeted treatment would significantly impact these patient populations. With a focus on clinical relevance in TBI, we synthesize current knowledge concerning UCP2 and its potential neuroprotective role and apply this body of knowledge to current and potential treatment modalities.
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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.