ArticleAging cell2014
Glyoxalase I reduces glycative and oxidative stress and prevents age-related endothelial dysfunction through modulation of endothelial nitric oxide synthase phosphorylation.
Article in Aging cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 63 citations in OpenAlex.
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- Effect of theophylline on vascular tissue in a model of oxidative stress induced by titanium dioxide nanoparticles.Toxicology research · 2025Article
- Mechanisms of cellular senescence-induced vascular aging: evidence of senotherapeutic strategies.The journal of cardiovascular aging · 2025Article
- Antioxidative and Antiglycative Stress Activities of Selenoglutathione Diselenide.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Determination of Nutrient Intake and Dietary Antioxidant Capacity in Autism Spectrum Disorder: A Case-Control Study.Journal of autism and developmental disorders · 2024Article
- Effect of Fluoride on the Expression of 8-Hydroxy-2'-Deoxyguanosine in the Blood, Kidney, Liver, and Brain of Rats.Biological trace element research · 2023Article
- Methylglyoxal in the Brain: From Glycolytic Metabolite to Signalling Molecule.Molecules (Basel, Switzerland) · 2022Review
- Apolipoprotein C3-Rich Low-Density Lipoprotein Induces Endothelial Cell Senescence via FBXO31 and Its Inhibition by Sesamol In Vitro and In Vivo.Biomedicines · 2022Article
- Multi-omics of human plasma reveals molecular features of dysregulated inflammation and accelerated aging in schizophrenia.Molecular psychiatry · 2022Article
- Organelle stress and glycation in kidney disease.Glycoconjugate journal · 2021Review
- Protection of Polyphenols against Glyco-Oxidative Stress: Involvement of Glyoxalase Pathway.Antioxidants (Basel, Switzerland) · 2020Article
- Dicarbonyl Stress and S-Glutathionylation in Cerebrovascular Diseases: A Focus on Cerebral Cavernous Malformations.Antioxidants (Basel, Switzerland) · 2020Review
- Article
- Glycine increases glyoxalase-1 function by promoting nuclear factor erythroid 2-related factor 2 translocation into the nucleus of kidney cells of streptozotocin-induced diabetic rats.Journal of diabetes investigation · 2019Article
- Cardiovascular Disease-Related Serum Proteins in Workers Occupationally Exposed to Polycyclic Aromatic Hydrocarbons.Toxicological sciences : an official journal of the Society of Toxicology · 2019Article
- Combined LDL and VLDL Electronegativity Correlates with Coronary Heart Disease Risk in Asymptomatic Individuals.Journal of clinical medicine · 2019Article
- Review
- Antioxidant Capacity and Behavioral Relevance of a Polyphenolic Extract ofOxidative medicine and cellular longevity · 2019Article
- Molecular Factors of Hypochlorite Tolerance in the Hypersaline Archaeon Haloferax volcanii.Genes · 2018Article
- Alterations of proteome, mitochondrial dynamic and autophagy in the hypothalamus during activity-based anorexia.Scientific reports · 2018Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endothelial dysfunction is a major contributor to cardiovascular disease (CVD), particularly in elderly people. Studies have demonstrated the role of glycation in endothelial dysfunction in nonphysiological models, but the physiological role of glycation in age-related endothelial dysfunction has been poorly addressed. Here, to investigate how vascular glycation affects age-related endothelial function, we employed rats systemically overexpressing glyoxalase I (GLO1), which detoxifies methylglyoxal (MG), a representative precursor of glycation. Four groups of rats were examined, namely young (13 weeks old), mid-age (53 weeks old) wild-type, and GLO1 transgenic (WT/GLO1 Tg) rats. Age-related acceleration in glycation was attenuated in GLO1 Tg rats, together with lower aortic carboxymethyllysine (CML) and urinary 8-hydroxydeoxyguanosine (8-OHdG) levels. Age-related impairment of endothelium-dependent vasorelaxation was attenuated in GLO1 Tg rats, whereas endothelium-independent vasorelaxation was not different between WT and GLO1 Tg rats. Nitric oxide (NO) production was decreased in mid-age WT rats, but not in mid-age GLO1 Tg rats. Age-related inactivation of endothelial NO synthase (eNOS) due to phosphorylation of eNOS on Thr495 and dephosphorylation on Ser1177 was ameliorated in GLO1 Tg rats. In vitro, MG increased phosphorylation of eNOS (Thr495) in primary human aortic endothelial cells (HAECs), and overexpression of GLO1 decreased glycative stress and phosphorylation of eNOS (Thr495). Together, GLO1 reduced age-related endothelial glycative and oxidative stress, altered phohphorylation of eNOS, and attenuated endothelial dysfunction. As a molecular mechanism, GLO1 lessened inhibitory phosphorylation of eNOS (Thr495) by reducing glycative stress. Our study demonstrates that blunting glycative stress prevents the long-term impact of endothelial dysfunction on vascular aging.
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