Trial reportMolecular metabolism2018
Compensatory mechanisms for methylglyoxal detoxification in experimental & clinical diabetes.
Trial report in Molecular metabolism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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.
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
49 citing papers in PubMed, 69 citations in OpenAlex.
- Six-Month Periodic Fasting in Patients With Type 2 Diabetes and Diabetic Nephropathy: A Proof-of-Concept Study.The Journal of clinical endocrinology and metabolism · 2022Trial
- Glyoxalase 1 loss reduces fatty liver but impairs glucose handling in male mice.Physiological reports · 2026Article
- Microbiota and Methylglyoxal-Derived AGEs: Implications in Ageing and Age-Related Disease.Life (Basel, Switzerland) · 2026Review
- Comprehensive in silico analysis of eggNOG-annotated orthologous genes infers functional dynamics and energy metabolism in the microbiome of Abutilon fruticosum.BMC plant biology · 2026Article
- Reactive carbonyl species in health and chronic disease: from methylglyoxal to an integrative network of metabolic regulation.Cardiovascular diabetology · 2026Review
- Systems genomics reveals age- and sex-dependent metabolic dysregulation fromPhysiological genomics · 2026Article
- Glyoxalase 1 is a proadipogenic gene.The Journal of biological chemistry · 2025Article
- Cohort profile of the Heidelberg study on diabetes and complications HEIST-DiC.Scientific reports · 2025Article
- Metabolomics: Uncovering Insights into Obesity and Diabetes.International journal of molecular sciences · 2025Article
- Restoring Glutathione Homeostasis in Glycation-Related Eye Diseases: Mechanistic Insights and Therapeutic Interventions Beyond VEGF Inhibition.Antioxidants (Basel, Switzerland) · 2025Review
- A Comprehensive Review of Metabolic Dysfunction-Associated Steatotic Liver Disease: Its Mechanistic Development Focusing on Methylglyoxal and Counterbalancing Treatment Strategies.International journal of molecular sciences · 2025Review
- Fluorescent probes for sensing and visualizing methylglyoxal: progress, challenges, and perspectives.RSC advances · 2024Review
- The role of DNA damage in diabetic complications.Nature reviews. Endocrinology · 2024Article
- Factor XII signaling via uPAR-integrin β1 axis promotes tubular senescence in diabetic kidney disease.Nature communications · 2024Article
- Glucose Load Following Prolonged Fasting Increases Oxidative Stress- Linked Response in Individuals With Diabetic Complications.Diabetes care · 2024Article
- Loss of NAMPT and SIRT2 but not SIRT1 attenuate GLO1 expression and activity in human skeletal muscle.Redox biology · 2024Article
- Endogenous Cellular Metabolite Methylglyoxal Induces DNA-Protein Cross-Links in Living Cells.ACS chemical biology · 2024Article
- Genetic Variants Influence the Development of Diabetic Neuropathy.International journal of molecular sciences · 2024Review
- Deletion of Glyoxalase 1 Exacerbates Acetaminophen-Induced Hepatotoxicity in Mice.Antioxidants (Basel, Switzerland) · 2024Article
- Accumulation of Non-Pathological Liver Fat Is Associated with the Loss of Glyoxalase I Activity in Humans.Metabolites · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesThe deficit of Glyoxalase I (Glo1) and the subsequent increase in methylglyoxal (MG) has been reported to be one the five mechanisms by which hyperglycemia causes diabetic late complications. Aldo-keto reductases (AKR) have been shown to metabolize MG; however, the relative contribution of this superfamily to the detoxification of MG in vivo, particularly within the diabetic state, remains unknown.
methodsCRISPR/Cas9-mediated genome editing was used to generate a Glo1 knock-out (Glo1
resultsGlo1
conclusionsThese data suggest that in the absence of GLO1, AKR can effectively compensate to prevent the accumulation of MG. The combination of metabolic, enzymatic, and genetic factors, therefore, may provide a better means of identifying patients who are at risk for the development of late complications caused by elevated levels of MG.
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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.