ReviewThe Journal of pharmacology and experimental therapeutics2017
Mitochondrial-Based Therapeutics for the Treatment of Spinal Cord Injury: Mitochondrial Biogenesis as a Potential Pharmacological Target.
Review in The Journal of pharmacology and experimental therapeutics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 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.
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Who cites it
63 citing papers in PubMed, 106 citations in OpenAlex.
- Drp1 in M1 layer V GABAergic neurons orchestrates rTMS-mediated motor restoration and analgesia after spinal cord injury.Experimental & molecular medicine · 2026Article
- Kainate-induced ATP release contributes to spinal excitotoxicity that is attenuated by purinergic blockade.Frontiers in neurology · 2026Article
- SOX Genes in Spinal Cord Injury: Redefining Neural Stem Cell Regeneration Strategies.Molecular neurobiology · 2025Review
- X inactive-specific transcript regulates mitochondrial function and neuronal differentiation of stem cellsWorld journal of stem cells · 2025Article
- Formoterol alters chemokine expression and ameliorates pain behaviors after moderate spinal cord injury in female mice.The Journal of pharmacology and experimental therapeutics · 2025Article
- Evolution of Lipid Metabolism in the Injured Mouse Spinal Cord.Journal of neurotrauma · 2025Article
- Antioxidant nanozymes: current status and future perspectives in spinal cord injury treatments.Theranostics · 2025Review
- Mitochondrial-targeted therapies in traumatic brain injury: From bench to bedside.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Machine learning-driven prediction model for cuproptosis-related genes in spinal cord injury: construction and experimental validation.Frontiers in neurology · 2025Article
- Therapeutic potential of melatonin-pretreated human dental pulp stem cells (hDPSCs) in an animal model of spinal cord injury.Scientific reports · 2024Article
- Activation of the 5-HT1A Receptor by Eltoprazine Restores Mitochondrial and Motor Deficits in aInternational journal of molecular sciences · 2024Article
- Targeted Therapy of Spinal Cord Injury: Inhibition of Apoptosis Is a Promising Therapeutic Strategy.Molecular neurobiology · 2024Review
- GIP attenuates neuronal oxidative stress by regulating glucose uptake in spinal cord injury of rat.CNS neuroscience & therapeutics · 2024Article
- Horizontal mitochondrial transfer as a novel bioenergetic tool for mesenchymal stromal/stem cells: molecular mechanisms and therapeutic potential in a variety of diseases.Journal of translational medicine · 2024Review
- 5-HTFrontiers in cellular neuroscience · 2024Article
- Immediate administration of hTERT-MSCs-IDO1-EVs reduces hypoalbuminemia after spinal cord injury.Veterinary research forum : an international quarterly journal · 2024Article
- Syntaphilin Inactivation Can Enhance Axonal Mitochondrial Transport to Improve Spinal Cord Injury.Molecular neurobiology · 2023Review
- Role of DNA methylation during recovery from spinal cord injury with and without βExperimental neurology · 2023Article
- Mitochondrial dysfunction as a target in spinal cord injury: intimate correlation between pathological processes and therapeutic approaches.Neural regeneration research · 2023Review
- Photobiomodulation provides neuroprotection through regulating mitochondrial fission imbalance in the subacute phase of spinal cord injury.Neural regeneration research · 2023Article
3 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Spinal cord injury (SCI) is characterized by an initial trauma followed by a progressive cascade of damage referred to as secondary injury. A hallmark of secondary injury is vascular disruption leading to vasoconstriction and decreased oxygen delivery, which directly reduces the ability of mitochondria to maintain homeostasis and leads to loss of ATP-dependent cellular functions, calcium overload, excitotoxicity, and oxidative stress, further exacerbating injury. Restoration of mitochondria dysfunction during the acute phases of secondary injury after SCI represents a potentially effective therapeutic strategy. This review discusses the past and present pharmacological options for the treatment of SCI as well as current research on mitochondria-targeted approaches. Increased antioxidant activity, inhibition of the mitochondrial permeability transition, alternate energy sources, and manipulation of mitochondrial morphology are among the strategies under investigation. Unfortunately, many of these tactics address single aspects of mitochondrial dysfunction, ultimately proving largely ineffective. Therefore, this review also examines the unexplored therapeutic efficacy of pharmacological enhancement of mitochondrial biogenesis, which has the potential to more comprehensively improve mitochondrial function after SCI.
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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.