ArticleIn vitro cellular & developmental biology. Animal2015
Advanced glycation end products induce oxidative stress and mitochondrial dysfunction in SH-SY5Y cells.
Article in In vitro cellular & developmental biology. Animal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 36 citations in OpenAlex.
- AGEs-RAGE Axis and Mitochondrial-Derived Peptides in Advanced Chronic Kidney Disease: Interconnected Pathways Beyond Inflammation and Nutrition.Antioxidants (Basel, Switzerland) · 2026Article
- An overview on glycation: molecular mechanisms, impact on proteins, pathogenesis, and inhibition.Biophysical reviews · 2024Review
- Article
- PHPB Attenuated Cognitive Impairment in Type 2 Diabetic KK-Ay Mice by Modulating SIRT1/Insulin Signaling Pathway and Inhibiting Generation of AGEs.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Advanced glycation end products modulate electrophysiological remodeling of right ventricular outflow tract cardiomyocytes: A novel target for diabetes-related ventricular arrhythmogenesis.Physiological reports · 2022Article
- AGE/Non-AGE Glycation: An Important Event in Rheumatoid Arthritis Pathophysiology.Inflammation · 2022Review
- In Vitro Methodologies to Study the Role of Advanced Glycation End Products (AGEs) in Neurodegeneration.Nutrients · 2022Review
- Glyoxal-Lysine Dimer, an Advanced Glycation End Product, Induces Oxidative Damage and Inflammatory Response by Interacting with RAGE.Antioxidants (Basel, Switzerland) · 2021Article
- MicroRNAs and Oxidative Stress: An Intriguing Crosstalk to Be Exploited in the Management of Type 2 Diabetes.Antioxidants (Basel, Switzerland) · 2021Review
- The Isothiocyanate Sulforaphane Depends on the Nrf2/γ-GCL/GSH Axis to Prevent Mitochondrial Dysfunction in Cells Exposed to Methylglyoxal.Neurochemical research · 2021Article
- A Bibenzyl Component Moscatilin Mitigates Glycation-Mediated Damages in an SH-SY5Y Cell Model of Neurodegenerative Diseases through AMPK Activation and RAGE/NF-Molecules (Basel, Switzerland) · 2020Article
- Role and Mechanisms of RAGE-Ligand Complexes and RAGE-Inhibitors in Cancer Progression.International journal of molecular sciences · 2020Review
- Does Protein Glycation Impact on the Drought-Related Changes in Metabolism and Nutritional Properties of Mature Pea (International journal of molecular sciences · 2020Article
- Changes in Cell Cycle and Up-Regulation of Neuronal Markers During SH-SY5Y Neurodifferentiation by Retinoic Acid are Mediated by Reactive Species Production and Oxidative Stress.Molecular neurobiology · 2017Article
- Astragaloside IV, a Natural PPARγ Agonist, Reduces Aβ Production in Alzheimer's Disease Through Inhibition of BACE1.Molecular neurobiology · 2017Article
- Receptor-mediated toxicity of human amylin fragment aggregated by short- and long-term incubations with copper ions.Molecular and cellular biochemistry · 2017Article
- Glucose availability determines silver nanoparticles toxicity in HepG2.Journal of nanobiotechnology · 2015Article
- Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study aimed to investigate the direct effects of advanced glycation end products (AGEs) on the mitochondrial structure and function of SH-SY5Y cells and the possible molecular mechanism(s) underlying mitochondria dysfunction by AGEs. SH-SY5Y cells were cultured in 400 μg/ml of AGE-bovine serum albumin (BSA) for 24 h, and changes in the mitochondrial function of SH-SY5Y cells were analysed as follows. Reactive oxygen species (ROS) were detected using 2',7'-dichlorodihydrofluorescein diacetate molecular probes. Mitochondrial membrane potential (ΔΨm) was determined by flow cytometry using fluorescent probes. The expression of cytochrome c (Cyt c) protein level was assessed by Western blotting. Mitochondrial structures were observed by transmission electron microscopy. Our results showed that AGE-BSA induced an increase in ROS levels, a decrease in mitochondrial ΔΨm, and the release of Cyt c from mitochondria in SH-SY5Y cells. The mitochondria of SH-SY5Y cells showed remarkable swelling and vacuolisation, but these changes were recovered after pretreatment with neutralising anti-receptor for advanced glycation end products (RAGE) antibody. Our results suggested that AGE-BSA induced mitochondrial dysfunction in SH-SY5Y cells through RAGE pathways. Thus, AGEs are potential mechanistic links between diabetes mellitus and Alzheimer's disease.
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