ReviewAntioxidants & redox signaling2015
Function and Mechanisms of Autophagy in Brain and Spinal Cord Trauma.
Review in Antioxidants & redox signaling, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers, 4 of them syntheses that pooled it.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
133 citing papers in PubMed, 4 syntheses or guidelines pooled it, 231 citations in OpenAlex.
- Endoplasmic Reticulum Stress in Spinal Cord Injury: Pathological Roles, Molecular Targets, and Emerging Treatments: A Systematic Review.Molecular neurobiology · 2026Pooled it
- A bibliometric analysis of the research hotspots and frontiers related to cell death in spinal cord injury.Frontiers in neurology · 2023Pooled it
- Bibliometric analysis and visualized study of research on autophagy in ischemic stroke.Frontiers in pharmacology · 2023Pooled it
- The utilization of small non-mammals in traumatic brain injury research: A systematic review.CNS neuroscience & therapeutics · 2021Pooled it
- Baicalin and CNS-related diseases: new insights into neuroprotective potentials based on underlying mechanisms.Biochemistry and biophysics reports · 2026Review
- Cel-LDH dual-functional nanotherapy simultaneously promotes microglial efferocytosis and alleviates neuronal apoptosis for spinal cord injury recovery.Journal of nanobiotechnology · 2026Article
- Cell apoptosis in ischemic stroke: Focus on lipid metabolism.Neural regeneration research · 2026Article
- 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
- Pterostilbene Promotes Spinal Cord Injury Recovery by Inhibiting Ferroptosis via Keap1/Nrf2/SLC7A11/GPX4 Axis Activation.Antioxidants (Basel, Switzerland) · 2026Article
- Roles and regulatory mechanisms of autophagy in the pathology of spinal cord injury.Burns & trauma · 2026Review
- Copper-regulated cell death after spinal cord injury: evidence boundaries for non-coding RNA, epigenetics and cuproptosis.Frontiers in molecular neuroscience · 2026Review
- Inhibition of the P2Y2 Receptor Promotes Facial Nerve Function by Enhancing Neuron Autophagy.Current neuropharmacology · 2026Article
- LncRNA MIR155HG suppresses cell apoptosis by activating autophagy via miR-7036b-3p/GPNMB axis and AMPK/mTOR signaling in spinal cord injury.Non-coding RNA research · 2025Article
- Review
- Inhibition of autophagy-lysosomal function exacerbates microglial and monocyte lipid metabolism reprograming and dysfunction after brain injury.Research square · 2025Article
- Inhibition of autophagy-lysosomal function exacerbates microglial and monocyte lipid metabolism reprograming and dysfunction after brain injury.bioRxiv : the preprint server for biology · 2025Article
- Advances in ERK Signaling Pathway in Traumatic Brain Injury: Mechanisms and Therapeutic Potential.Neurochemical research · 2025Review
- Therapeutic Potential of MCC950 in Restoring Autophagy and Cognitive Function in STZ-Induced Rat Model of Alzheimer's Disease.Molecular neurobiology · 2025Article
73 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
4 authors at 1 institution in 1 country.
Funding
Abstract
significanceTraumatic brain injury (TBI) and spinal cord injury (SCI) are major causes of death and long-term disability worldwide. Despite important pathophysiological differences between these disorders, in many respects, mechanisms of injury are similar. During both TBI and SCI, some cells are directly mechanically injured, but more die as a result of injury-induced biochemical changes (secondary injury). Autophagy, a lysosome-dependent cellular degradation pathway with neuroprotective properties, has been implicated both clinically and experimentally in the delayed response to TBI and SCI. However, until recently, its mechanisms and function remained unknown, reflecting in part the difficulty of isolating autophagic processes from ongoing cell death and other cellular events. RECENT ADVANCES: Emerging data suggest that depending on the location and severity of traumatic injury, autophagy flux--defined as the progress of cargo through the autophagy system and leading to its degradation--may be either increased or decreased after central nervous system trauma. CRITICAL ISSUES: While increased autophagy flux may be protective after mild injury, after more severe trauma inhibition of autophagy flux may contribute to neuronal cell death, indicating disruption of autophagy as a part of the secondary injury mechanism. FUTURE DIRECTIONS: Augmentation and/or restoration of autophagy flux may provide a potential therapeutic target for treatment of TBI and SCI. Development of those treatments will require thorough characterization of changes in autophagy flux, its mechanisms and function over time after injury.
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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.