ArticlePloS one2014
Temporal dynamics of glyoxalase 1 in secondary neuronal injury.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Exploratory Application of Neuropharmacometabolomics in Severe Childhood Traumatic Brain Injury.Critical care medicine · 2018Trial
- Ryanodine receptor 2-mediated calcium leak is associated with increased glyoxalase I in the aging brain.JCI insight · 2025Article
- Hyperglycemic effects on limbs tingling and twisting sensations.Frontiers in neurology · 2025Review
- On the importance of the innervation of the human cervical longitudinal ligaments at vertebral level.Surgical and radiologic anatomy : SRA · 2020Article
- Review
- Comparative Examination of Temporal Glyoxalase 1 Variations Following Perforant Pathway Transection, Excitotoxicity, and Controlled Cortical Impact Injury.Neurotoxicity research · 2018Article
- Ethyl pyruvate does not require microglia for mediating neuroprotection after excitotoxic injury.CNS neuroscience & therapeutics · 2017Article
- AGEs and neurodegeneration: the Nrf2/glyoxalase-1 interaction.Oncotarget · 2017Article
- Glutathione-Dependent Detoxification Processes in Astrocytes.Neurochemical research · 2015Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEnhanced glycolysis leads to elevated levels of the toxic metabolite methylglyoxal which contributes to loss of protein-function, metabolic imbalance and cell death. Neurons were shown being highly susceptible to methylglyoxal toxicity. Glyoxalase 1 as an ubiquitous enzyme reflects the main detoxifying enzyme of methylglyoxal and underlies changes during aging and neurodegeneration. However, little is known about dynamics of Glyoxalase 1 following neuronal lesions so far.
methodsTo determine a possible involvement of Glyoxalase 1 in acute brain injury, we analysed the temporal dynamics of Glyoxalase 1 distribution and expression by immunohistochemistry and Western Blot analysis. Organotypic hippocampal slice cultures were excitotoxically (N-methyl-D-aspartate, 50 µM for 4 hours) lesioned in vitro (5 minutes to 72 hours). Additionally, permanent middle cerebral artery occlusion was performed (75 minutes to 60 days).
resultsWe found (i) a predominant localisation of Glyoxalase 1 in endothelial cells in non-lesioned brains (ii) a time-dependent up-regulation and re-distribution of Glyoxalase 1 in neurons and astrocytes and (iii) a strong increase in Glyoxalase 1 dimers after neuronal injury (24 hours to 72 hours) when compared to monomers of the protein.
conclusionsThe high dynamics of Glyoxalase 1 expression and distribution following neuronal injury may indicate a novel role of Glyoxalase 1.
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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.