ArticleMolecular neurobiology2017
Autophagy Inhibition Favors Survival of Rubrospinal Neurons After Spinal Cord Hemisection.
Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.
- Endoplasmic Reticulum Stress in Spinal Cord Injury: Pathological Roles, Molecular Targets, and Emerging Treatments: A Systematic Review.Molecular neurobiology · 2026Pooled it
- Activin A enhances neurofunctional recovery following traumatic spinal cord injury by inhibiting autophagy.Neural regeneration research · 2026Article
- The role of autophagy in spinal cord injury: Mechanisms, crosstalk, and therapeutic strategies.Neural regeneration research · 2026Article
- Platelet-rich plasma-primed bone marrow mesenchymal stem cell-derived exosomes inhibit neuronal apoptosis and autophagy, and promote nerve regeneration via the miR-29a-3p/PTEN/PI3K/Akt/mTOR axis after spinal cord injury.Journal of molecular histology · 2026Article
- Roles and regulatory mechanisms of autophagy in the pathology of spinal cord injury.Burns & trauma · 2026Review
- Thoracic Spinal Cord Contusion Impacts on Lumbar Enlargement: Molecular Insights.Molecular neurobiology · 2025Article
- MLKL-USP7-UBA52 signaling is indispensable for autophagy in brain through maintaining ubiquitin homeostasis.Autophagy · 2025Article
- Crosstalk Between Cell Death and Spinal Cord Injury: Neurology and Therapy.Molecular neurobiology · 2024Review
- Targeted Therapy of Spinal Cord Injury: Inhibition of Apoptosis Is a Promising Therapeutic Strategy.Molecular neurobiology · 2024Review
- Progress of Ginsenoside Rb1 in neurological disorders.Frontiers in pharmacology · 2024Review
- Tibolone Improves Locomotor Function in a Rat Model of Spinal Cord Injury by Modulating Apoptosis and Autophagy.International journal of molecular sciences · 2023Article
- Mitochondrial dysfunction as a target in spinal cord injury: intimate correlation between pathological processes and therapeutic approaches.Neural regeneration research · 2023Review
- Autophagy regulation combined with stem cell therapy for treatment of spinal cord injury.Neural regeneration research · 2023Review
- Spinal cord injury: molecular mechanisms and therapeutic interventions.Signal transduction and targeted therapy · 2023Review
- Neuroprotective Roles of Apelin-13 in Neurological Diseases.Neurochemical research · 2023Review
- Different Ways to Die: Cell Death Pathways and Their Association With Spinal Cord Injury.Neurospine · 2023Article
- Advances in molecular therapies for targeting pathophysiology in spinal cord injury.Expert opinion on therapeutic targets · 2023Review
- Targeting autophagy process in center nervous trauma.Frontiers in neuroscience · 2023Review
- Restoration of ER proteostasis attenuates remote apoptotic cell death after spinal cord injury by reducing autophagosome overload.Cell death & disease · 2022Article
- Progression in translational research on spinal cord injury based on microenvironment imbalance.Bone research · 2022Review
Corrections and comments
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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
Spinal cord injuries (SCIs) are devastating conditions of the central nervous system (CNS) for which there are no restorative therapies. Neuronal death at the primary lesion site and in remote regions that are functionally connected to it is one of the major contributors to neurological deficits following SCI.Disruption of autophagic flux induces neuronal death in many CNS injuries, but its mechanism and relationship with remote cell death after SCI are unknown. We examined the function and effects of the modulation of autophagy on the fate of axotomized rubrospinal neurons in a rat model of spinal cord dorsal hemisection (SCH) at the cervical level. Following SCH, we observed an accumulation of LC3-positive autophagosomes (APs) in the axotomized neurons 1 and 5 days after injury. Furthermore, this accumulation was not attributed to greater initiation of autophagy but was caused by a decrease in AP clearance, as demonstrated by the build-up of p62, a widely used marker of the induction of autophagy. In axotomized rubrospinal neurons, the disruption of autophagic flux correlated strongly with remote neuronal death and worse functional recovery. Inhibition of AP biogenesis by 3-methyladenine (3-MA) significantly attenuated remote degeneration and improved spontaneous functional recovery, consistent with the detrimental effects of autophagy in remote damage after SCH. Collectively, our results demonstrate that autophagic flux is blocked in axotomized neurons on SCI and that the inhibition of AP formation improves their survival. Thus, autophagy is a promising target for the development of therapeutic interventions in the treatment of SCIs.
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