ReviewInternational journal of molecular sciences2017
The Role of Glyoxalase-I (Glo-I), Advanced Glycation Endproducts (AGEs), and Their Receptor (RAGE) in Chronic Liver Disease and Hepatocellular Carcinoma (HCC).
Review in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
40 citing papers in PubMed, 63 citations in OpenAlex.
- A Citrus and Pomegranate Complex Reduces Methylglyoxal in Healthy Elderly Subjects: Secondary Analysis of a Double-Blind Randomized Cross-Over Clinical Trial.International journal of molecular sciences · 2023Trial
- AMarine drugs · 2022Trial
- [Scutellarin improves metabolic dysfunction-associated steatotic liver disease in rats by regulating MMP7 and LCN2].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- R-α-Lipoic Acid Attenuates Acetaminophen-Induced Acute Liver Injury by Reducing Oxidative Stress, Inflammation, and Mitochondrial Damage in Mice.Drug design, development and therapy · 2026Article
- AGEs-RAGE manipulates tumor intrinsic pERK/Sp1/IL6 pathway and reprograms macrophage to promote intrahepatic cholangiocarcinoma progression.Translational oncology · 2025Article
- Advanced Glycation End Products in Disease Development and Potential Interventions.Antioxidants (Basel, Switzerland) · 2025Review
- Review
- 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
- L-Theanine Extends the Lifespan ofFoods (Basel, Switzerland) · 2025Article
- Meloxicam mitigated methylglyoxal-induced glycative stress in rats.Iranian journal of basic medical sciences · 2025Article
- Natural medicines for treating liver fibrosis by modulating post-translational modifications.Frontiers in pharmacology · 2025Review
- Pyridoxamine reduces inflammatory and microcirculatory abnormalities in metabolic dysfunction-associated steatohepatitis and modulates key factors in the hepatic AGE/ALE signaling pathway.Frontiers in physiology · 2025Article
- Punicic acid alleviates methylglyoxal-induced oocyte dysfunction during in vitro maturation in mouse species.PloS one · 2025Article
- Phloroglucinol ameliorated methylglyoxal induced harmful effects in rats.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Association between Mediterranean Diet and Advanced Glycation End Products in University Students: A Cross-Sectional Study.Nutrients · 2024Article
- Deletion of Glyoxalase 1 Exacerbates Acetaminophen-Induced Hepatotoxicity in Mice.Antioxidants (Basel, Switzerland) · 2024Article
- Review
- Structures of Toxic Advanced Glycation End-Products Derived from Glyceraldehyde, A Sugar Metabolite.Biomolecules · 2024Review
- Prediction of CAF-related genes in immunotherapy and drug sensitivity in hepatocellular carcinoma: a multi-database analysis.Genes and immunity · 2024Article
- Screening immune-related blood biomarkers for DKD-related HCC using machine learning.Frontiers in immunology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glyoxalase-I (Glo-I) and glyoxalase-II (Glo-II) comprise the glyoxalase system and are responsible for the detoxification of methylglyoxal (MGO). MGO is formed non-enzymatically as a by-product, mainly in glycolysis, and leads to the formation of advanced glycation endproducts (AGEs). AGEs bind to their receptor, RAGE, and activate intracellular transcription factors, resulting in the production of pro-inflammatory cytokines, oxidative stress, and inflammation. This review will focus on the implication of the Glo-I/AGE/RAGE system in liver injury and hepatocellular carcinoma (HCC). AGEs and RAGE are upregulated in liver fibrosis, and the silencing of RAGE reduced collagen deposition and the tumor growth of HCC. Nevertheless, data relating to Glo-I in fibrosis and cirrhosis are preliminary. Glo-I expression was found to be reduced in early and advanced cirrhosis with a subsequent increase of MGO-levels. On the other hand, pharmacological modulation of Glo-I resulted in the reduced activation of hepatic stellate cells and therefore reduced fibrosis in the CCl₄-model of cirrhosis. Thus, current research highlighted the Glo-I/AGE/RAGE system as an interesting therapeutic target in chronic liver diseases. These findings need further elucidation in preclinical and clinical studies.
Indexed as
Identifiers
What OpenQuestion holds
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.