ArticleNeurocritical care2017
Autophagy Biomarkers Beclin 1 and p62 are Increased in Cerebrospinal Fluid after Traumatic Brain Injury.
Article in Neurocritical care, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 54 citations in OpenAlex.
- Bixafen Induces Programmed Cell Death inJournal of fungi (Basel, Switzerland) · 2026Article
- Gestational chronic intermittent hypoxia triggers maternal inflammation and disrupts placental stress responses.American journal of physiology. Cell physiology · 2025Article
- BECLIN-1/BECN1 at the barrier: a gatekeeper of epithelial and endothelial homeostasis.Autophagy reports · 2025Review
- Mechanisms and therapeutic potential of hyperbaric oxygen inducing autophagy in cerebral ischemia-reperfusion injury.American journal of translational research · 2025Review
- Traumatic brain injury heterogeneity affects cell death and autophagy.Experimental brain research · 2024Article
- Autophagy inhibitor 3-methyladenine attenuates renal injury in streptozotocin-induced diabetic mice.Iranian journal of basic medical sciences · 2024Article
- Massive Solubility Changes in Neuronal Proteins upon Simulated Traumatic Brain Injury Reveal the Role of Shockwaves in Irreversible Damage.Molecules (Basel, Switzerland) · 2023Article
- Altered diffusivity of the subarachnoid cisterns in the rat brain following neurological disorders.Biomedical journal · 2023Article
- Autophagy machinery plays an essential role in traumatic brain injury-induced apoptosis and its related behavioral abnormalities in mice: focus onFrontiers in physiology · 2023Article
- Investigating p62 Concentrations in Cerebrospinal Fluid of Patients with Dementia: A Potential Autophagy Biomarker In Vivo?Brain sciences · 2022Article
- Improper Proteostasis: Can It Serve as Biomarkers for Neurodegenerative Diseases?Molecular neurobiology · 2022Review
- Review
- Article
- Pediatric Traumatic Brain Injury: An Update on Preclinical Models, Clinical Biomarkers, and the Implications of Cerebrovascular Dysfunction.Journal of central nervous system disease · 2022Review
- Mitophagy in neurological disorders.Journal of neuroinflammation · 2021Review
- Deficiency in Androgen Receptor Aggravates Traumatic Brain Injury-Induced Pathophysiology and Motor Deficits in Mice.Molecules (Basel, Switzerland) · 2021Article
- Iron Metabolism Disorders for Cognitive Dysfunction After Mild Traumatic Brain Injury.Frontiers in neuroscience · 2021Review
- Article
- Spermidine Exhibits Protective Effects Against Traumatic Brain Injury.Cellular and molecular neurobiology · 2020Article
- Extracellular Vesicles miRNA Cargo for Microglia Polarization in Traumatic Brain Injury.Biomolecules · 2020Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAutophagy is a process that recycles damaged proteins and organelles. Beclin 1 is involved in the nucleation phase, while p62 is consumed during the elongation phase. We hypothesized that these autophagy biomarkers are increased in cerebrospinal fluid (CSF) after traumatic brain injury (TBI) in children and associated with unfavorable outcome.
methodsThirty children with severe TBI had CSF collected on days 1, 3, and 7. Patients without TBI or meningoencephalitis served as controls. Beclin 1 and p62 were measured by ELISA. Outcome was assigned 6 months after injury (Glasgow Outcome Scale score; GOS).
resultsMean and peak CSF beclin 1 and p62 levels were increased compared to controls (P < 0.05). Peak p62 levels were higher in patients with unfavorable versus favorable outcome (0.79 ± 1.03 vs. 0.17 ± 0.54 ng/ml, respectively; mean ± SD, P = 0.002) and were independently associated with outcome when controlling for age and initial Glasgow Coma Scale score (P = 0.019; AUC 0.88, 95% CI 0.76, 1.00).
conclusionsBeclin 1 and p62 are increased in CSF after TBI, suggesting increased autophagy with impairment of, and/or exceeding the capacity for, autophagic flux. The association of increased p62 with unfavorable outcome suggests that autophagy in excess of the capacity to clear degradation products may be deleterious after TBI.
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