ArticleNeural regeneration research2016
Time representation of mitochondrial morphology and function after acute spinal cord injury.
Article in Neural regeneration research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed.
- Spatiotemporal disarray of inflammatory microenvironment following spinal cord injury.Neural regeneration research · 2026Article
- Spinal cord injury induces mitochondrial dysfunction and metabolic reprogramming in non-regenerativeiScience · 2026Article
- Polydatin for treating spinal cord injury: Multiple mechanisms and challenges.Journal of pharmaceutical analysis · 2026Review
- Phosphatidylserine Decarboxylase Regulates Retinal Ganglion Cell Neurite Outgrowth with Altered Somal Membrane Fluidics and Mitochondrial Morphology.Biomolecules · 2026Article
- Circulating microRNA Profiles in Acute Spinal Cord Injury: Evidence for Distinct Plasma Signatures Compared with Polytrauma Patients.International journal of molecular sciences · 2025Article
- Enhancement of spinal cord injury repair in rats using photo-crosslinked GelMA hydrogel combined with mitochondrial transplantation.Bioengineering & translational medicine · 2025Article
- Mitochondrial dynamics reveal potential to facilitate axonal regeneration after spinal cord injury.Journal of translational medicine · 2025Review
- Mitochondrial Transplantation/Transfer: Promising Therapeutic Strategies for Spinal Cord Injury.Journal of orthopaedic translation · 2025Review
- Poly(glycerol succinate) hydrogel promotes spinal cord repair by regulating bio-energetic activity in severe injury.Materials today. Bio · 2025Article
- Ligand-Screened Cerium-Based MOF Microcapsules Promote Nerve Regeneration via Mitochondrial Energy Supply.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Photobiomodulation provides neuroprotection through regulating mitochondrial fission imbalance in the subacute phase of spinal cord injury.Neural regeneration research · 2023Article
- Photobiomodulation augments the effects of mitochondrial transplantation in the treatment of spinal cord injury in rats by facilitating mitochondrial transfer to neurons via Connexin 36.Bioengineering & translational medicine · 2023Article
- Nrf2 Activation: Involvement in Central Nervous System Traumatic Injuries. A Promising Therapeutic Target of Natural Compounds.International journal of molecular sciences · 2022Review
- Mitochondrial function in spinal cord injury and regeneration.Cellular and molecular life sciences : CMLS · 2022Review
- Progression in translational research on spinal cord injury based on microenvironment imbalance.Bone research · 2022Review
- Mitochondrial Transplantation Attenuates Neural Damage and Improves Locomotor Function After Traumatic Spinal Cord Injury in Rats.Frontiers in neuroscience · 2022Article
- Photobiomodulation promotes repair following spinal cord injury by restoring neuronal mitochondrial bioenergeticsFrontiers in pharmacology · 2022Article
- CD157 in bone marrow mesenchymal stem cells mediates mitochondrial production and transfer to improve neuronal apoptosis and functional recovery after spinal cord injury.Stem cell research & therapy · 2021Article
- Mitochondrial Behavior in Axon Degeneration and Regeneration.Frontiers in aging neuroscience · 2021Review
- Mitochondria focused neurotherapeutics for spinal cord injury.Experimental neurology · 2020Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Changes in mitochondrial morphology and function play an important role in secondary damage after acute spinal cord injury. We recorded the time representation of mitochondrial morphology and function in rats with acute spinal cord injury. Results showed that mitochondria had an irregular shape, and increased in size. Mitochondrial cristae were disordered and mitochondrial membrane rupture was visible at 2-24 hours after injury. Fusion protein mitofusin 1 expression gradually increased, peaked at 8 hours after injury, and then decreased to its lowest level at 24 hours. Expression of dynamin-related protein 1, amitochondrial fission protein, showed the opposite kinetics. At 2-24 hours after acute spinal cord injury, malondialdehyde content, cytochrome c levels and caspase-3 expression were increased, but glutathione content, adenosine triphosphate content, Na(+)-K(+)-ATPase activity and mitochondrial membrane potential were gradually reduced. Furthermore, mitochondrial morphology altered during the acute stage of spinal cord injury. Fusion was important within the first 8 hours, but fission played a key role at 24 hours. Oxidative stress was inhibited, biological productivity was diminished, and mitochondrial membrane potential and permeability were reduced in the acute stage of injury. In summary, mitochondrial apoptosis is activated when the time of spinal cord injury is prolonged.
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