ReviewBiomolecules2021
Intracellular Toxic AGEs (TAGE) Triggers Numerous Types of Cell Damage.
Review in Biomolecules, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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
32 citing papers in PubMed, 45 citations in OpenAlex.
- The Interplay Between Immunometabolism and Neuroinflammation in Alzheimer's Disease.Biomolecules · 2026Review
- The brain's sweet spot: why microglia can run on fructose metabolism.Frontiers in immunology · 2026Review
- AGE-RAGE Axis and Cardiovascular Diseases: Pathophysiologic Mechanisms and Prospects for Clinical Applications.Cardiovascular drugs and therapy · 2025Review
- Mechanism and implications of advanced glycation end products (AGE) and its receptor RAGE axis as crucial mediators linking inflammation and obesity.Molecular biology reports · 2025Review
- Article
- A Comprehensive Review of Metabolic Dysfunction-Associated Steatotic Liver Disease: Its Mechanistic Development Focusing on Methylglyoxal and Counterbalancing Treatment Strategies.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
- Meloxicam mitigated methylglyoxal-induced glycative stress in rats.Iranian journal of basic medical sciences · 2025Article
- Exploring the Role of Tripeptides in Wound Healing and Skin Regeneration: A Comprehensive Review.International journal of medical sciences · 2025Review
- 4-HNE-induced cellular dysfunction from lipid peroxidation: a potential therapeutic target in diabetic cardiomyopathy.Frontiers in cell and developmental biology · 2025Review
- Toxic AGEs (TAGE) Cause Lifestyle-Related Diseases.Antioxidants (Basel, Switzerland) · 2024Review
- Exploring the Exposome Spectrum: Unveiling Endogenous and Exogenous Factors in Non-Communicable Chronic Diseases.Diseases (Basel, Switzerland) · 2024Review
- Advanced Glycation End-Products Acting as Immunomodulators for Chronic Inflammation, Inflammaging and Carcinogenesis in Patients with Diabetes and Immune-Related Diseases.Biomedicines · 2024Review
- Accumulation of Intracellular Protein Advanced Glycation End Products Alters Cellular Homeostasis for Protein Clearance in Pancreatic Ductal Epithelial Cells.Biochemistry · 2024Article
- Metabolic Syndrome and Biotherapeutic Activity of Dairy (Cow and Buffalo) Milk Proteins and Peptides: Fast Food-Induced Obesity Perspective-A Narrative Review.Biomolecules · 2024Review
- An overview on glycation: molecular mechanisms, impact on proteins, pathogenesis, and inhibition.Biophysical reviews · 2024Review
- Structures of Toxic Advanced Glycation End-Products Derived from Glyceraldehyde, A Sugar Metabolite.Biomolecules · 2024Review
- Article
- Protein Advanced Glycation End Products and Their Implications in Pancreatic Cancer.Cancer prevention research (Philadelphia, Pa.) · 2023Review
- Impact of Polyphenols on Inflammatory and Oxidative Stress Factors in Diabetes Mellitus: Nutritional Antioxidants and Their Application in Improving Antidiabetic Therapy.Biomolecules · 2023Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
The habitual intake of large amounts of sugar, which has been implicated in the onset/progression of lifestyle-related diseases (LSRD), induces the excessive production of glyceraldehyde (GA), an intermediate of sugar metabolism, in neuronal cells, hepatocytes, and cardiomyocytes. Reactions between GA and intracellular proteins produce toxic advanced glycation end-products (toxic AGEs, TAGE), the accumulation of which contributes to various diseases, such as Alzheimer's disease, non-alcoholic steatohepatitis, and cardiovascular disease. The cellular leakage of TAGE affects the surrounding cells via the receptor for AGEs (RAGE), thereby promoting the onset/progression of LSRD. We demonstrated that the intracellular accumulation of TAGE triggered numerous cellular disorders, and also that TAGE leaked into the extracellular space, thereby increasing extracellular TAGE levels in circulating fluids. Intracellular signaling and the production of reactive oxygen species are affected by extracellular TAGE and RAGE interactions, which, in turn, facilitate the intracellular generation of TAGE, all of which may contribute to the pathological changes observed in LSRD. In this review, we discuss the relationships between intracellular TAGE levels and numerous types of cell damage. The novel concept of the "TAGE theory" is expected to open new perspectives for research into LSRD.
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Registered trials
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.