ReviewFrontiers in neuroscience2015
Methylglyoxal, the dark side of glycolysis.
Review in Frontiers in neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 292 papers, 1 of them a synthesis that pooled it.
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
292 citing papers in PubMed, 1 synthesis or guideline pooled it, 533 citations in OpenAlex.
- Dietary patterns and biomarkers of oxidative stress and inflammation: A systematic review of observational and intervention studies.Redox biology · 2021Pooled it
- Activated protein C promotes hematopoietic stem and progenitor cell quiescence and engraftment.EMBO molecular medicine · 2026Article
- Unveiling the "Glycolysis-Lactate-Lactylation" Axis: A Novel Target in Ischemic Cerebrovascular Disease.Neuroscience bulletin · 2026Review
- Reactive aldehyde species-mediated neuropathic pain in spinal cord injury: Mechanisms and therapeutic opportunities.Neural regeneration research · 2026Article
- Complex Contributions of Methylglyoxal to Pain, Axon Degeneration, and Diabetic Peripheral Neuropathy.Journal of neurochemistry · 2026Review
- Microbiota and Methylglyoxal-Derived AGEs: Implications in Ageing and Age-Related Disease.Life (Basel, Switzerland) · 2026Review
- Review
- Host methylglyoxal activates theProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Txnrd2 loss in skeletal muscle causes muscle atrophy and drives leanness and obesity resistance.Redox biology · 2026Article
- Synergistic interactions between glycogen and trehalose mediate adaptation to the stationary phase inJournal of bacteriology · 2026Article
- Increased Serum GLO-1 Levels Are Associated With the Pathophysiology and Development of Obsessive-Compulsive Disorder: Findings From a Case-Control Study.Health science reports · 2026Article
- Lactate metabolism-driven lactylation: paradoxical modulation of intestinal inflammation and malignancy.Journal of translational medicine · 2026Review
- Astrocyte-Neuron Crosstalk in Hypertension: Mechanisms and Therapeutic Significance.Reviews in cardiovascular medicine · 2026Review
- Integrative analyses of dicarbonyls and advanced glycation end-products with multiomic profiles across tissue, plasma and stool samples reveal methylglyoxal accumulation in colon cancer.Free radical biology & medicine · 2026Article
- Methylglyoxal Affects Dopamine Homeostasis in SH-SY5Y Cells Through the Modulation of miR-190a and miR-214.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Glycolytic Specialization Shapes Neuronal Physiology and FunctionbioRxiv : the preprint server for biology · 2026Article
- Methylglyoxal-modification of NLRP3 interrupts NLRP3-NEK7 interaction diminishing inflammasome activation and neuroinflammation.Journal of neuroinflammation · 2026Article
- Sirtuin 2 Regulates Histone Glycation as a Semi-deglycase.Biochemistry · 2026Article
- The three pathways of advanced glycation end product synthesis: Hodge, Namiki, and Wolff - a clinically oriented mechanistic synthesis with network-based implications.Frontiers in endocrinology · 2026Review
- Polyphenol-based modulation of the Glo1-Nrf2-RAGE axis in diabetes and neurodegeneration: mechanistic evidence, translational constraints, and critical appraisal.Frontiers in pharmacology · 2026Review
232 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
3 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glucose is the main energy substrate for the brain. There is now extensive evidence indicating that the metabolic profile of neural cells with regard to glucose utilization and glycolysis rate is not homogenous, with a marked propensity for glycolytic glucose processing in astrocytes compared to neurons. Methylglyoxal, a highly reactive dicarbonyl compound, is inevitably formed as a by-product of glycolysis. Methylglyoxal is a major cell-permeant precursor of advanced glycation end-products (AGEs), which are associated with several pathologies including diabetes, aging and neurodegenerative diseases. In normal situations, cells are protected against methylglyoxal toxicity by different mechanisms and in particular the glyoxalase system, which represents the most important pathway for the detoxification of methylglyoxal. While the neurotoxic effects of methylglyoxal and AGEs are well characterized, our understanding the glyoxalase system in the brain is more scattered. Considering the high energy requirements (i.e., glucose) of the brain, one should expect that the cerebral glyoxalase system is adequately fitted to handle methylglyoxal toxicity. This review focuses on our actual knowledge on the cellular aspects of the glyoxalase system in brain cells, in particular with regard to its activity in astrocytes and neurons. A main emerging concept is that these two neural cell types have different and energetically adapted glyoxalase defense mechanisms which may serve as protective mechanism against methylglyoxal-induced cellular damage.
Indexed as
Identifiers
What OpenQuestion holds
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.