ArticleFrontiers in cellular neuroscience2018
Cell Specific Changes of Autophagy in a Mouse Model of Contusive Spinal Cord Injury.
Article in Frontiers in cellular neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- Automated segmentation of neurons and spinal cord structures in immunofluorescence images using SpineDL.Scientific reports · 2026Article
- The role of autophagy in spinal cord injury: Mechanisms, crosstalk, and therapeutic strategies.Neural regeneration research · 2026Article
- Inhibition of the P2Y2 Receptor Promotes Facial Nerve Function by Enhancing Neuron Autophagy.Current neuropharmacology · 2026Article
- Article
- The Role of Autophagy in Long-term Effects of Spinal Cord Injury: Does Exosome Change the Autophagy Process and Vice Versa?Advanced pharmaceutical bulletin · 2025Review
- Article
- Review
- Reanalysis of Published Histological Data Can Help to Characterize Neuronal Death After Spinal Cord Injury.International journal of molecular sciences · 2025Article
- Galactin-3 regulation of CDC42 promotes neuronal autophagy following spinal cord injury.Frontiers in cellular neuroscience · 2025Article
- Autophagy markers LC3 and p62 in aging lumbar motor neurons.Experimental gerontology · 2024Article
- The Role of Exosomes from Mesenchymal Stem Cells in Spinal Cord Injury: A Systematic Review.International journal of stem cells · 2024Review
- Article
- Article
- Enhancement of oligodendrocyte autophagy alleviates white matter injury and cognitive impairment induced by chronic cerebral hypoperfusion in rats.Acta pharmaceutica Sinica. B · 2023Article
- Autophagic degradation of CNS myelin maintains axon integrity.Cell stress · 2022Article
- The Proteostasis Network: A Global Therapeutic Target for Neuroprotection after Spinal Cord Injury.Cells · 2022Review
- MicroRNA-138-5p Targets Pro-Apoptotic Factors and Favors Neural Cell Survival: Analysis in the Injured Spinal Cord.Biomedicines · 2022Article
- Progression in translational research on spinal cord injury based on microenvironment imbalance.Bone research · 2022Review
- Insulin-like growth factor 1 promotes neurological functional recovery after spinal cord injury through inhibition of autophagy via the PI3K/Akt/mTOR signaling pathway.Experimental and therapeutic medicine · 2021Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy is an essential process of cellular waist clearance that becomes altered following spinal cord injury (SCI). Details on these changes, including timing after injury, underlying mechanisms, and affected cells, remain controversial. Here we present a characterization of autophagy in the mice spinal cord before and after a contusive SCI. In the undamaged spinal cord, analysis of LC3 and Beclin 1 autophagic markers reveals important differences in basal autophagy between neurons, oligodendrocytes, and astrocytes and even within cell populations. Following moderate contusion, western blot analyses of LC3 indicates that autophagy increases to a maximum at 7 days post injury (dpi), whereas unaltered Beclin 1 expression and increase of p62 suggests a possible blockage of autophagosome clearance. Immunofluorescence analyses of LC3 and Beclin 1 provide additional details that reveal a complex, cell-specific scenario. Autophagy is first activated (1 dpi) in the severed axons, followed by a later (7 dpi) accumulation of phagophores and/or autophagosomes in the neuronal soma without signs of increased initiation. Oligodendrocytes and reactive astrocytes also accumulate phagophores and autophagosomes at 7 dpi, but whereas the accumulation in astrocytes is associated with an increased autophagy initiation, it seems to result from a blockage of the autophagic flux in oligodendrocytes. Comparison with previous studies highlights the complex and heterogeneous autophagic responses induced by the SCI, leading in many cases to contradictory results and interpretations. Future studies should consider this complexity in the design of therapeutic interventions based on the modulation of autophagy to treat SCI.
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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.