ArticleScientific reports2019
Intracellular toxic advanced glycation end-products in cardiomyocytes may cause cardiovascular disease.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.
- Higher skin autofluorescence detection using AGE-Reader™ technology as a measure of increased tissue accumulation of advanced glycation end products in dialysis patients with diabetes: a meta-analysis.Journal of artificial organs : the official journal of the Japanese Society for Artificial Organs · 2021Pooled it
- AGE-RAGE Axis and Cardiovascular Diseases: Pathophysiologic Mechanisms and Prospects for Clinical Applications.Cardiovascular drugs and therapy · 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
- The roles of advanced glycation end products in cardiovascular diseases: from mechanisms to therapeutic strategies.Frontiers in cardiovascular 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
- Small molecule mediators of host-T. cruzi-environment interactions in Chagas disease.PLoS pathogens · 2024Review
- 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
- The Role of Advanced Glycation End-Product Levels Measured by Skin Autofluorescence in the Development of Mitral Annular Calcification.Journal of cardiovascular development and disease · 2023Article
- 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
- 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
- Plasma concentrations of advanced glycation end-products and colorectal cancer risk in the EPIC study.Carcinogenesis · 2021Article
- Intracellular Toxic AGEs (TAGE) Triggers Numerous Types of Cell Damage.Biomolecules · 2021Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiovascular disease (CVD) is a lifestyle-related disease (LSRD) and one of the largest public health issues. Risk factors for CVD correlate with an excessive intake of glucose and/or fructose, which has been shown to induce the production of advanced glycation end-products (AGEs). We previously identified AGEs derived from glyceraldehyde and named them toxic AGEs (TAGE) due to their cytotoxicities and relationship with LSRD. We also reported that extracellular TAGE in the vascular system may promote CVD and that serum TAGE levels are associated with risk factors for CVD. The mechanisms responsible for the onset and/or progression of CVD by extracellular TAGE or the above risk factors involve vascular disorders. In the present study, we revealed that rat primary cultured cardiomyocytes generated intracellular TAGE, which decreased beating rates and induced cell death. LC3-II/LC3-I, a factor of autophagy, also decreased. Although intracellular TAGE may be targets of degradation as cytotoxic proteins via autophagy, they may inhibit autophagy. Furthermore, the mechanisms by which intracellular TAGE decrease beating rates and induce cell death may involve the suppression of autophagy. The present results suggest that intracellular TAGE are generated in cardiomyocytes and directly damage them, resulting in CVD.
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Registered trials
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