ArticleArteriosclerosis, thrombosis, and vascular biology2008
Role of advanced glycation end products with oxidative stress in resistance artery dysfunction in type 2 diabetic mice.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 85 citations in OpenAlex.
- Trial
- Coconut Milk-Derived Bioactive Peptides as Multifunctional Agents Against Hyperglycemia, Oxidative Stress, and Glycation: An Integrated Experimental and Computational Study.International journal of molecular sciences · 2025Article
- Downregulated calmodulin expression contributes to endothelial cell impairment in diabetes.Acta pharmacologica Sinica · 2023Article
- RAGE signaling regulates the progression of diabetic complications.Frontiers in pharmacology · 2023Review
- Plasmacytoid dendritic cells contribute to vascular endothelial dysfunction in type 2 diabetes.Frontiers in cardiovascular medicine · 2023Article
- Accumulation of fluorescent advanced glycation end products and carboxymethyl-lysine in human cortical and trabecular bone.Bone reports · 2022Article
- Alternate Day Fasting Improves Endothelial Function in Type 2 Diabetic Mice: Role of Adipose-Derived Hormones.Frontiers in cardiovascular medicine · 2022Article
- Cellular and molecular effects of hyperglycemia on ion channels in vascular smooth muscle.Cellular and molecular life sciences : CMLS · 2021Review
- Mechanisms underlying suppression of noradrenaline-induced contraction by prolonged treatment with advanced glycation end-products in organ-cultured rat carotid artery.Pflugers Archiv : European journal of physiology · 2020Article
- Amplification of the COX/TXS/TP receptor pathway enhances uridine diphosphate-induced contraction by advanced glycation end products in rat carotid arteries.Pflugers Archiv : European journal of physiology · 2019Article
- Association between Subclinical Atherosclerosis Markers and the Level of Accumulated Advanced Glycation End-Products in the Skin of Patients with Diabetes.Journal of atherosclerosis and thrombosis · 2018Observational
- Essential Role of IL-12 in Angiogenesis in Type 2 Diabetes.The American journal of pathology · 2017Article
- Advanced glycation end-products decreases expression of endothelial nitric oxide synthase through oxidative stress in human coronary artery endothelial cells.Cardiovascular diabetology · 2017Article
- Abnormal myosin phosphatase targeting subunit 1 phosphorylation and actin polymerization contribute to impaired myogenic regulation of cerebral arterial diameter in the type 2 diabetic Goto-Kakizaki rat.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017Article
- Implication of advanced glycation end products (Ages) and their receptor (Rage) on myocardial contractile and mitochondrial functions.Glycoconjugate journal · 2016Review
- Developmental conditioning of endothelium-derived hyperpolarizing factor-mediated vasorelaxation.Journal of hypertension · 2016Article
- Advanced Glycation End Products Induce Obesity and Hepatosteatosis in CD-1 Wild-Type Mice.BioMed research international · 2016Article
- Tumor necrosis factor inhibition increases the revascularization of ischemic hind-limbs in diabetic mice.Naunyn-Schmiedeberg's archives of pharmacology · 2015Article
- Nuclear factor kappa B inhibition improves conductance artery function in type 2 diabetic mice.Diabetes/metabolism research and reviews · 2015Article
- Advanced Glycation End Products Impair Voltage-Gated K+ Channels-Mediated Coronary Vasodilation in Diabetic Rats.PloS one · 2015Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
objectiveType 2 diabetes is associated with increased advanced glycation end product (AGE) formation and vasculopathy. We hypothesized that AGEs contribute to resistance artery dysfunction. METHODS AND
resultsType 2 diabetic db(-)/db(-) (diabetic) and nondiabetic db(-)/db(+) (control) mice were treated with the AGE inhibitor (aminoguanidine: 50 mg/Kg/d) for 3 months. Isolated mesenteric resistance arteries (MRAs) were mounted in an arteriograph. Pressure-induced myogenic tone (MT) was increased in diabetic mice but was unaffected by aminoguanidine treatment. Phenylephrine-induced contraction and nitric oxide donor-induced endothelium-independent relaxation were similar in all groups. In diabetic mice, endothelium-dependent relaxation in response to shear-stress or acetylcholine was altered and was associated with reduced eNOS protein and mRNA expression. Aminoguanidine treatment improved endothelial function and restored eNOS expression. AGE formation and hypoxia markers (plasminogen activator inhibitor 1 and Bnip3) were increased in MRA from diabetic mice and normalized with Aminoguanidine. Primary cultured endothelial cells (ECs) isolated from resistance arteries subjected to high glucose for 48 hours showed decreased eNOS expression and phosphorylation in response to calcium ionophore. High glucose decreased antioxidant protein (MnSOD) and increased prooxidant proteins (gp91phox) expression leading to increased oxidative stress generation, as assessed by DHE staining and endothelial NADH/NADPH oxidase activity. The preincubation of ECs with aminoguanidine restored eNOS-phosphorylation and expression as well as the balance between pro- and antioxidant factors induced by high glucose.
conclusionsWe provide evidence of a link between AGEs, oxidative stress, and resistance artery EC dysfunction in type 2 diabetic mice. Thus, AGEs and oxidative stress may be a potential target for overcoming diabetic microvessels complications.
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