ArticleDiabetologia2012
Protection against methylglyoxal-derived AGEs by regulation of glyoxalase 1 prevents retinal neuroglial and vasodegenerative pathology.
Article in Diabetologia, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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Who cites it
70 citing papers in PubMed, 150 citations in OpenAlex.
- Targeting Glyoxalase-1 Pathway with Natural Compounds: A Translational Strategy to Reduce Dicarbonyl Stress and Prevent Chronic Diseases.Life (Basel, Switzerland) · 2026Review
- Glycation metabolites predict incident age-related comorbidities and mortality in older people with HIV.GeroScience · 2026Article
- Advanced Glycation End Products and Metabolic-Mechanical Coupling in Diabetic Retinopathy.Clinical ophthalmology (Auckland, N.Z.) · 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
- Does Gut Microbial Methylglyoxal Metabolism Impact Human Physiology?Antioxidants (Basel, Switzerland) · 2025Review
- Anserine reduces mortality in experimental sepsis by preventing methylglyoxal-induced capillary leakage.EBioMedicine · 2025Article
- Genetic context modulates aging and degeneration in the murine retina.Molecular neurodegeneration · 2025Article
- Subacute exposure to apigenin induces changes in protein synthesis in the liver of Swiss mice.Frontiers in physiology · 2025Article
- Methylglyoxal: A Key Factor for Diabetic Retinopathy and Its Effects on Retinal Damage.Biomedicines · 2024Review
- Glycative stress as a cause of macular degeneration.Progress in retinal and eye research · 2024Review
- Genetic context modulates aging and degeneration in the murine retina.bioRxiv : the preprint server for biology · 2024Article
- Molecular Assessment of Methylglyoxal-Induced Toxicity and Therapeutic Approaches in Various Diseases: Exploring the Interplay with the Glyoxalase System.Life (Basel, Switzerland) · 2024Review
- Article
- Dieckol, Derived from the Edible Brown AlgaeAntioxidants (Basel, Switzerland) · 2023Article
- Methylglyoxal and Its Adducts: Induction, Repair, and Association with Disease.Chemical research in toxicology · 2022Review
- Nutraceutical Prevention of Diabetic Complications-Focus on Dicarbonyl and Oxidative Stress.Current issues in molecular biology · 2022Review
- Review on Chemical Constituents of Schizonepeta tenuifolia Briq. and Their Pharmacological EffectsMolecules (Basel, Switzerland) · 2022Review
- Methylglyoxal and glyoxalase 1-a metabolic stress pathway-linking hyperglycemia to the unfolded protein response and vascular complications of diabetes.Clinical science (London, England : 1979) · 2022Article
- Rapid pretreatment for multi-sample analysis of advanced glycation end products and their role in nephropathy.Journal of clinical biochemistry and nutrition · 2022Article
- An anthracenecarboximide-guanidine fluorescent probe for selective detection of glyoxals under weak acidic conditions.RSC advances · 2022Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors at 8 institutions in 4 countries.
Funding
Abstract
aims/hypothesisMethylglyoxal (MG) is an important precursor for AGEs. Normally, MG is detoxified by the glyoxalase (GLO) enzyme system (including component enzymes GLO1 and GLO2). Enhanced glycolytic metabolism in many cells during diabetes may overpower detoxification capacity and lead to AGE-related pathology. Using a transgenic rat model that overexpresses GLO1, we investigated if this enzyme can inhibit retinal AGE formation and prevent key lesions of diabetic retinopathy.
methodsTransgenic rats were developed by overexpression of full length GLO1. Diabetes was induced in wild-type (WT) and GLO1 rats and the animals were killed after 12 or 24 weeks of hyperglycaemia. N ε)-(Carboxyethyl)lysine (CEL), N(ε)-(carboxymethyl)lysine (CML) and MG-derived-hydroimidazalone-1 (MG-H1) were determined by immunohistochemistry and by ultra-performance liquid chromatography tandem mass spectrometry (UPLC-MSMS). Müller glia dysfunction was determined by glial fibrillary acidic protein (GFAP) immunoreactivity and by spatial localisation of the potassium channel Kir4.1. Acellular capillaries were quantified in retinal flat mounts.
resultsGLO1 overexpression prevented CEL and MG-H1 accumulation in the diabetic retina when compared with WT diabetic counterparts (p < 0.01). Diabetes-related increases in Müller glial GFAP levels and loss of Kir4.1 at the vascular end-feet were significantly prevented by GLO1 overexpression (p < 0.05) at both 12- and 24-week time points. GLO1 diabetic animals showed fewer acellular capillaries than WT diabetic animals (p < 0.001) at 24 weeks' diabetes. CONCLUSIONS/
interpretationDetoxification of MG reduces AGE adduct accumulation, which, in turn, can prevent formation of key retinal neuroglial and vascular lesions as diabetes progresses. MG-derived AGEs play an important role in diabetic retinopathy.
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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.