ArticleDiabetology & metabolic syndrome2020
Impact of intracellular toxic advanced glycation end-products (TAGE) on murine myoblast cell death.
Article in Diabetology & metabolic syndrome, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 30 citations in OpenAlex.
- A Reassessment of Sarcopenia from a Redox Perspective as a Basis for Preventive and Therapeutic Interventions.International journal of molecular sciences · 2025Review
- The Advanced Glycation End-Products (AGE)-Receptor for AGE System (RAGE): An Inflammatory Pathway Linking Obesity and Cardiovascular Diseases.International journal of molecular sciences · 2025Review
- Laboratory-based Biomarkers for Risk Prediction, Auxiliary Diagnosis and Post-operative Follow-up of Osteoporotic Fractures.Current osteoporosis reports · 2025Review
- The role of AGEs in skeletal muscle atrophy and the beneficial effects of exercise.Frontiers in medicine · 2025Review
- Slot Blot- and Electrospray Ionization-Mass Spectrometry/Matrix-Assisted Laser Desorption/Ionization-Mass Spectrometry-Based Novel Analysis Methods for the Identification and Quantification of Advanced Glycation End-Products in the Urine.International journal of molecular sciences · 2024Article
- Slot Blot Analysis of Intracellular Glyceraldehyde-Derived Advanced Glycation End Products Using a Novel Lysis Buffer and Polyvinylidene Difluoride Membrane.Bio-protocol · 2024Article
- Generation and Accumulation of Various Advanced Glycation End-Products in Cardiomyocytes May Induce Cardiovascular Disease.International journal of molecular sciences · 2024Review
- Unveiling the Threat of Maternal Advanced Glycation End Products to Fetal Muscle: Palmitoleic Acid to the Rescue.Nutrients · 2024Article
- Glycative stress inhibits hypertrophy and impairs cell membrane integrity in overloaded mouse skeletal muscle.Journal of cachexia, sarcopenia and muscle · 2024Article
- Structures of Toxic Advanced Glycation End-Products Derived from Glyceraldehyde, A Sugar Metabolite.Biomolecules · 2024Review
- Potential of the Novel Slot Blot Method with a PVDF Membrane for Protein Identification and Quantification in Kampo Medicines.Membranes · 2023Article
- Utilization of Macroalgae for the Production of Bioactive Compounds and Bioprocesses Using Microbial Biotechnology.Microorganisms · 2023Review
- Is the Novel Slot Blot a Useful Method for Quantification of Intracellular Advanced Glycation End-Products?Metabolites · 2023Review
- Involvement of Intracellular TAGE and the TAGE-RAGE-ROS Axis in the Onset and Progression of NAFLD/NASH.Antioxidants (Basel, Switzerland) · 2023Review
- Serum Level of Heat Shock Protein 70 in Patients with Type 2 Diabetes Mellitus in Basrah, Iraq.Archives of Razi Institute · 2022Article
- Association of skin autofluorescence with low bone density/osteoporosis and osteoporotic fractures in type 2 diabetes mellitus.Journal of diabetes · 2022Article
- Effects of Toxic AGEs (TAGE) on Human Health.Cells · 2022Review
- Intracellular Toxic Advanced Glycation End-Products May Induce Cell Death and Suppress Cardiac Fibroblasts.Metabolites · 2022Article
- Article
- Pyridoxamine and Aminoguanidine Attenuate the Abnormal Aggregation of β-Tubulin and Suppression of Neurite Outgrowth by Glyceraldehyde-Derived Toxic Advanced Glycation End-Products.Frontiers in pharmacology · 2022Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSarcopenia is a progressive condition that is characterized by decreases in skeletal muscle mass and function. Although sarcopenia is associated with lifestyle-related diseases (LSRD), the mechanisms underlying cell death in myoblasts, which differentiate to myotubes, remain unclear. We previously designated glyceraldehyde (an intermediate of glucose/fructose metabolism)-derived advanced glycation end-products (AGEs) as toxic AGEs (TAGE) because of their cytotoxicity and involvement in LSRD, and hypothesized that TAGE contribute to cell death in myoblasts.
methodsC2C12 cells, which are murine myoblasts, were treated with 0, 0.5, 1, 1.5, and 2 mM glyceraldehyde for 24 h. Cell viability and intracellular TAGE were then assessed using 5-[2,4,-bis(sodioxysulfonyl)phenyl]-3-(2-methoxy-4-nitrophenyl)-2-(4-nitrophenyl)-2
resultsIn C2C12 cells treated with 1.5 and 2 mM glyceraldehyde, cell viability decreased to 47.7% (
conclusionIntracellular TAGE strongly induced cell death in C2C12 cells and may also induce myoblast cell death in LSRD model mice.
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