ArticleScientific reports2016
Mitochondrial fission is an acute and adaptive response in injured motor neurons.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 62 citations in OpenAlex.
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- Absence of the axon initial segment in sensory neuron enhances resistance to amyotrophic lateral sclerosis.Brain : a journal of neurology · 2025Article
- Knockout of the mitoribosome rescue factors Ict1 or Mtrfr is viable in zebrafish but not mice: compensatory mechanisms underlying each factor's loss.FEBS open bio · 2025Article
- Sex-specific decline in prefrontal cortex mitochondrial bioenergetics in aging baboons correlates with walking speed.Neurobiology of aging · 2025Article
- Pulsed Radiofrequency Relieves Neuropathic Pain by Repairing the Ultrastructural Damage of Chronically Compressed Dorsal Root Ganglion.Neuroscience insights · 2025Article
- Optineurin overexpression ameliorates neurodegeneration through regulating neuroinflammation and mitochondrial quality in a murine model of amyotrophic lateral sclerosis.Frontiers in aging neuroscience · 2025Article
- Extremely Low-Frequency Electromagnetic Field (ELF-EMF) Increases Mitochondrial Electron Transport Chain Activities and Ameliorates Depressive Behaviors in Mice.International journal of molecular sciences · 2024Article
- Sex-specific decline in prefrontal cortex mitochondrial bioenergetics in aging baboons correlates with walking speed.bioRxiv : the preprint server for biology · 2024Article
- Repeated cold stress, an animal model for fibromyalgia, elicits proprioceptor-induced chronic pain with microglial activation in mice.Journal of neuroinflammation · 2024Article
- Mdivi-1 Rescues Memory Decline in Scopolamine-Induced Amnesic Male Mice by Ameliorating Mitochondrial Dynamics and Hippocampal Plasticity.Molecular neurobiology · 2023Article
- Three-dimensional ultrastructure analysis of organelles in injured motor neuron.Anatomical science international · 2023Review
- Molecular mechanisms of neurite regeneration and repair: insights from C. elegans and Drosophila.Cell regeneration (London, England) · 2023Review
- The Effects of PP2A Disruption on ER-Mitochondria Contact and Mitochondrial Functions in Neuronal-like Cells.Biomedicines · 2023Article
- Axonal transport deficits in the pathogenesis of diabetic peripheral neuropathy.Frontiers in endocrinology · 2023Review
- How neurons maintain their axons long-term: an integrated view of axon biology and pathology.Frontiers in neuroscience · 2023Review
- Electrophilic Aldehyde 4-Hydroxy-2-Nonenal Mediated Signaling and Mitochondrial Dysfunction.Biomolecules · 2022Review
- Personalized Treatment for Infantile Ascending Hereditary Spastic Paralysis Based on In Silico Strategies.Molecules (Basel, Switzerland) · 2022Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Successful recovery from neuronal damage requires a huge energy supply, which is provided by mitochondria. However, the physiological relevance of mitochondrial dynamics in damaged neurons in vivo is poorly understood. To address this issue, we established unique bacterial artificial chromosome transgenic (BAC Tg) mice, which develop and function normally, but in which neuronal injury induces labelling of mitochondria with green fluorescent protein (GFP) and expression of cre recombinase. GFP-labelled mitochondria in BAC Tg mice appear shorter in regenerating motor axons soon after nerve injury compared with mitochondria in non-injured axons, suggesting the importance of increased mitochondrial fission during the early phase of nerve regeneration. Crossing the BAC Tg mice with mice carrying a floxed dynamin-related protein 1 gene (Drp1), which is necessary for mitochondrial fission, ablates mitochondrial fission specifically in injured neurons. Injury-induced Drp1-deficient motor neurons show elongated or abnormally gigantic mitochondria, which have impaired membrane potential and axonal transport velocity during the early phase after injury, and eventually promote neuronal death. Our in vivo data suggest that acute and prominent mitochondrial fission during the early stage after nerve injury is an adaptive response and is involved in the maintenance of mitochondrial and neuronal integrity to prevent neurodegeneration.
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