ReviewCells2019
Autophagy in Neurotrauma: Good, Bad, or Dysregulated.
Review in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
82 citing papers in PubMed.
- Snapin mediates neuronal PANoptosis after mild traumatic brain injury via HJournal of advanced research · 2026Article
- Acupuncture regulates mitochondrial homeostasis in traumatic brain injury: current evidence, mechanistic hypotheses, and translational challenges.Chinese medicine · 2026Review
- Dental Luting Cements and Peri-Implantitis: Molecular Mechanisms, Clinical Implications and the Role of Autophagy and Nanotechnology-A Narrative Review.Dentistry journal · 2026Review
- The role of autophagy in spinal cord injury: Mechanisms, crosstalk, and therapeutic strategies.Neural regeneration research · 2026Article
- Phagocytosis and neuroinflammation: orchestrating central nervous system homeostasis, repair, and the resolution of inflammation.Trends in neurosciences · 2026Review
- Autophagy activation by the Becn1Brain, behavior, and immunity · 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
- Microglial NLRC5 drives lysosomal dysfunction to disrupt autophagic flux and promote post-stroke neuroinflammation.Journal of neuroinflammation · 2025Article
- Histone H4K16 acetylation modification regulated autophagy and apoptosis in neuron after spinal cord injury.Scientific reports · 2025Article
- Inherited Genetic Variation in Parkinson's Disease: Convergence on Impaired Autophagosome-Lysosome Fusion Through the Altered Expression of mRNA Isoforms.Molecular neurobiology · 2025Article
- Research Progress on Regulating Autophagy in Traditional Chinese Medicine for the Treatment of Traumatic Brain Injury.ACS omega · 2025Review
- Advances in ERK Signaling Pathway in Traumatic Brain Injury: Mechanisms and Therapeutic Potential.Neurochemical research · 2025Review
- Inhibition of CD36 ameliorates mouse spinal cord injury by accelerating microglial lipophagy.Acta pharmacologica Sinica · 2025Article
- Reanalysis of Published Histological Data Can Help to Characterize Neuronal Death After Spinal Cord Injury.International journal of molecular sciences · 2025Article
- Traumatic brain injury and autophagy: a pilot study about the immunohistochemical expression of LC3B, Beclin 1, p62, and LAMP2A in human autoptic samples.Frontiers in molecular neuroscience · 2025Article
- The emerging role of cuproptosis in spinal cord injury.Frontiers in immunology · 2025Review
- Article
- Galactin-3 regulation of CDC42 promotes neuronal autophagy following spinal cord injury.Frontiers in cellular neuroscience · 2025Article
- Schwann Cells and Their Exosomes: Research Progress and Prospect in Spinal Cord Injury.Neural plasticity · 2025Review
- Chaperone-Mediated Autophagy Alleviates Cerebral Ischemia-Reperfusion Injury by Inhibiting P53-Mediated Mitochondria-Associated Apoptosis.Neurochemical research · 2024Article
22 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
2 authors.
Funding
Abstract
Autophagy is a physiological process that helps maintain a balance between the manufacture of cellular components and breakdown of damaged organelles and other toxic cellular constituents. Changes in autophagic markers are readily detectable in the spinal cord and brain following neurotrauma, including traumatic spinal cord and brain injury (SCI/TBI). However, the role of autophagy in neurotrauma remains less clear. Whether autophagy is good or bad is under debate, with strong support for both a beneficial and detrimental role for autophagy in experimental models of neurotrauma. Emerging data suggest that autophagic flux, a measure of autophagic degradation activity, is impaired in injured central nervous systems (CNS), and interventions that stimulate autophagic flux may provide neuroprotection in SCI/TBI models. Recent data demonstrating that neurotrauma can cause lysosomal membrane damage resulting in pathological autophagosome accumulation in the spinal cord and brain further supports the idea that the impairment of the autophagy-lysosome pathway may be a part of secondary injury processes of SCI/TBI. Here, we review experimental work on the complex and varied responses of autophagy in terms of both the beneficial and detrimental effects in SCI and TBI models. We also discuss the existing and developing therapeutic options aimed at reducing the disruption of autophagy to protect the CNS after injuries.
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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.