ArticleDiabetes2009
Advanced glycation end products in extracellular matrix proteins contribute to the failure of sensory nerve regeneration in diabetes.
Article in Diabetes, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.
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Who cites it
96 citing papers in PubMed, 182 citations in OpenAlex.
- Metabolic targeting by a small extracellular vesicle-based cellulose-GelMA hydrogel restores neurovascular regeneration in diabetic nerve injury.Bioactive materials · 2027Article
- Review
- The AGE-RAGE-DIAPH1 Axis in Type 2 Diabetes and Metabolic Dysfunction: From Carbonyl Stress to Diabetic Myocardial and Neuronal Injury.International journal of molecular sciences · 2026Review
- Nerve Growth Factor in Diabetes Mellitus: Pathophysiological Mechanisms, Biomarkers and Therapeutic Opportunities.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Molecular Framework of the Onset and Progression of Skeletal Muscle Aging.International journal of molecular sciences · 2025Review
- Menaquinone-7 Supplementation Increases Multiple Advanced Glycation End-Products and Oxidation Markers in Zucker Diabetic Fatty Rats.Nutrients · 2025Article
- Relationship between serum LDH levels and diabetic peripheral neuropathy in type 2 diabetic patients.Frontiers in endocrinology · 2025Article
- Hyperglycemic effects on limbs tingling and twisting sensations.Frontiers in neurology · 2025Review
- Cell response to extracellular matrix viscous energy dissipation outweighs high-rigidity sensing.Science advances · 2024Article
- Methylglyoxal: A Key Factor for Diabetic Retinopathy and Its Effects on Retinal Damage.Biomedicines · 2024Review
- An overview on glycation: molecular mechanisms, impact on proteins, pathogenesis, and inhibition.Biophysical reviews · 2024Review
- Article
- Dual Glyoxalase-1 and β-Klotho Gene-Activated Scaffold Reduces Methylglyoxal and Reprograms Diabetic Adipose-Derived Stem Cells: Prospects in Improved Wound Healing.Pharmaceutics · 2024Article
- The TRIM21-FOXD1-BCL-2 axis underlies hyperglycaemic cell death and diabetic tissue damage.Cell death & disease · 2023Article
- The Dynamics of Nerve Degeneration and Regeneration in a Healthy Milieu and in Diabetes.International journal of molecular sciences · 2023Review
- Fibronectin in hyperglycaemia and its potential use in the treatment of diabetic foot ulcers: A review.International wound journal · 2023Review
- Axonal transport deficits in the pathogenesis of diabetic peripheral neuropathy.Frontiers in endocrinology · 2023Review
- Hexokinase-linked glycolytic overload and unscheduled glycolysis in hyperglycemia-induced pathogenesis of insulin resistance, beta-cell glucotoxicity, and diabetic vascular complications.Frontiers in endocrinology · 2023Article
- Overground gait adaptability in older adults with type 2 diabetes in response to virtual targets and physical obstacles.PloS one · 2023Article
- AGE-RAGE axis culminates into multiple pathogenic processes: a central road to neurodegeneration.Frontiers in molecular neuroscience · 2023Review
36 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
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThe goal of this study was to characterize glycation adducts formed in both in vivo extracellular matrix (ECM) proteins of endoneurium from streptozotocin (STZ)-induced diabetic rats and in vitro by glycation of laminin and fibronectin with methylglyoxal and glucose. We also investigated the impact of advanced glycation end product (AGE) residue content of ECM on neurite outgrowth from sensory neurons. RESEARCH DESIGN AND
methodsGlycation, oxidation, and nitration adducts of ECM proteins extracted from the endoneurium of control and STZ-induced diabetic rat sciatic nerve (3-24 weeks post-STZ) and of laminin and fibronectin that had been glycated using glucose or methylglyoxal were examined by liquid chromatography with tandem mass spectrometry. Methylglyoxal-glycated or unmodified ECM proteins were used as substrata for dissociated rat sensory neurons as in vitro models of regeneration.
resultsSTZ-induced diabetes produced a significant increase in early glycation N(epsilon)-fructosyl-lysine and AGE residue contents of endoneurial ECM. Glycation of laminin and fibronectin by methylglyoxal and glucose increased glycation adduct residue contents with methylglyoxal-derived hydroimidazolone and N(epsilon)-fructosyl-lysine, respectively, of greatest quantitative importance. Glycation of laminin caused a significant decrease in both neurotrophin-stimulated and preconditioned sensory neurite outgrowth. This decrease was prevented by aminoguanidine. Glycation of fibronectin also decreased preconditioned neurite outgrowth, which was prevented by aminoguanidine and nerve growth factor.
conclusionsEarly glycation and AGE residue content of endoneurial ECM proteins increase markedly in STZ-induced diabetes. Glycation of laminin and fibronectin causes a reduction in neurotrophin-stimulated neurite outgrowth and preconditioned neurite outgrowth. This may provide a mechanism for the failure of collateral sprouting and axonal regeneration in diabetic neuropathy.
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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.