ArticleJournal of gastroenterology2008
Advanced glycation end products enhance the proliferation and activation of hepatic stellate cells.
Article in Journal of gastroenterology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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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
58 citing papers in PubMed, 107 citations in OpenAlex.
- Atorvastatin decreases serum levels of advanced glycation endproducts (AGEs) in nonalcoholic steatohepatitis (NASH) patients with dyslipidemia: clinical usefulness of AGEs as a biomarker for the attenuation of NASH.Journal of gastroenterology · 2010Trial
- Review
- Liver fibrosis risk: a silent threat in type 1 diabetes mellitus.Journal of endocrinological investigation · 2026Article
- Mechanism of liver fibrosis induced by life-long triclosan exposure in offspring rats: an adverse outcome pathway framework validated by in vivo and in vitro experiments.Archives of toxicology · 2026Article
- Hyperglycemia in Diabetes Drives Hepatic Fibrosis Through the Non-Enzymatic Function of HK2 and AGEs-mediated Matrix Stiffening.International journal of biological sciences · 2026Article
- Higher plasma dicarbonyl levels are associated with liver fibrosis in obese individuals.Diabetes, obesity & metabolism · 2025Article
- Association of serum lactate dehydrogenase levels with non-alcoholic fatty liver disease and advanced hepatic fibrosis in the United States: a cross-sectional study using NHANES data from 2007 to 2018.BMC gastroenterology · 2025Article
- 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
- Advanced Glycation End Products in Disease Development and Potential Interventions.Antioxidants (Basel, Switzerland) · 2025Review
- 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
- Advanced glycation end products and risk of mortality in patients with cirrhosis: a prospective cohort study.Scientific reports · 2025Article
- Natural medicines for treating liver fibrosis by modulating post-translational modifications.Frontiers in pharmacology · 2025Review
- Deletion of Glyoxalase 1 Exacerbates Acetaminophen-Induced Hepatotoxicity in Mice.Antioxidants (Basel, Switzerland) · 2024Article
- Deletion of Glyoxalase 1 exacerbates acetaminophen-induced hepatotoxicity in mice.bioRxiv : the preprint server for biology · 2023Article
- Novel Fluorometric Assay of Antiglycation Activity Based on Methylglyoxal-Induced Protein Carbonylation.Antioxidants (Basel, Switzerland) · 2023Article
- Dietary advanced glycation end products are associated with an increased risk of non-alcoholic fatty liver disease in Iranian adults.BMC endocrine disorders · 2023Article
- Involvement of Intracellular TAGE and the TAGE-RAGE-ROS Axis in the Onset and Progression of NAFLD/NASH.Antioxidants (Basel, Switzerland) · 2023Review
- Glyoxal-derived advanced glycation end-products, NMolecular biology reports · 2023Article
- A standardized pomegranate fruit extract ameliorates thioacetamide-induced liver fibrosis in rats via AGE-RAGE-ROS signaling.Heliyon · 2023Article
- Effects of Toxic AGEs (TAGE) on Human Health.Cells · 2022Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAdvanced glycation end products (AGEs), final reaction products of protein with sugars, are known to contribute to diabetes-related complications. We have recently demonstrated high levels of serum AGEs in patients with nonalcoholic steatohepatitis (NASH). However, direct evidence for the participation of AGEs in hepatic inflammation and fibrosis has not been shown. To explore the pathogenesis of NASH, we examined the biological infl uence of AGEs on hepatic stellate cells (HSCs) in vitro.
methodsAn established human HSC line, LI90, was exposed to a glyceraldehyde-derived-AGE (glycer-AGE), and the phenotypical changes of the LI90 cells were investigated. Intracellular formation of reactive oxygen species (ROS) was measured using a fl uorescent probe. Cell proliferation was examined by MTS assay. Fibrogenic marker gene expression was analyzed by quantitative real-time polymerase chain reaction. The production of monocyte chemoattractant protein 1 (MCP-1) was assessed by enzyme-linked immunosorbent assay.
resultsThe expression of AGE receptor was confirmed in LI90 cells at the mRNA and protein levels. In addition to increasing intracellular ROS generation, glycer-AGE upregulated fibrogenic genes such as those encoding for alpha-smooth muscle actin, transforming growth factor-beta1, and collagen type Ialpha2. The expression of MCP-1 mRNA in LI90 cells as well as its secretion into the culture medium was significantly increased in response to AGEs. These changes were attenuated by treatment with the antioxidant N-acetylcysteine.
conclusionsThese data indicate that AGEs induce ROS generation and intensify the proliferation and activation of HSCs, supporting the possibility that antioxidants may represent a promising treatment for prevention of the development of hepatic fibrosis in NASH.
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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.