ReviewWorld journal of hepatology2015
Contribution of the toxic advanced glycation end-products-receptor axis in nonalcoholic steatohepatitis-related hepatocellular carcinoma.
Review in World journal of hepatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 34 citations in OpenAlex.
- Review
- CDT1 is a Potential Therapeutic Target for the Progression of NAFLD to HCC and the Exacerbation of Cancer.Current genomics · 2025Article
- Dietary advanced glycation end-products (dAGEs) are not associated with the risk of cancer incidence. A systematic review and meta-analysis of prospective cohort studies.Food science & nutrition · 2024Article
- 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
- Dietary intake of advanced glycation endproducts and risk of hepatobiliary cancers: A multinational cohort study.International journal of cancer · 2021Article
- Intracellular Toxic AGEs (TAGE) Triggers Numerous Types of Cell Damage.Biomolecules · 2021Review
- Increase of α-dicarbonyls in liver and receptor for advanced glycation end products on immune cells are linked to nonalcoholic fatty liver disease and liver cancer.Oncoimmunology · 2021Article
- Review
- Toxic AGEs (TAGE) theory: a new concept for preventing the development of diseases related to lifestyle.Diabetology & metabolic syndrome · 2020Review
- Impact of intracellular toxic advanced glycation end-products (TAGE) on murine myoblast cell death.Diabetology & metabolic syndrome · 2020Article
- Review
- Hyperglycemia Associated Metabolic and Molecular Alterations in Cancer Risk, Progression, Treatment, and Mortality.Cancers · 2019Review
- Intracellular toxic advanced glycation end-products in cardiomyocytes may cause cardiovascular disease.Scientific reports · 2019Article
- Role of AGEs in the progression and regression of atherosclerotic plaques.Glycoconjugate journal · 2018Review
- Role of Advanced Glycation End Products in Carcinogenesis and their Therapeutic Implications.Current pharmaceutical design · 2018Review
- Generation of glyceraldehyde-derived advanced glycation end-products in pancreatic cancer cells and the potential of tumor promotion.World journal of gastroenterology · 2017Article
- Toxic AGE (TAGE) Theory for the Pathophysiology of the Onset/Progression of NAFLD and ALD.Nutrients · 2017Review
- Impact of Dietary Fibers on Nutrient Management and Detoxification Organs: Gut, Liver, and Kidneys.Advances in nutrition (Bethesda, Md.) · 2016Review
- Iridoids are natural glycation inhibitors.Glycoconjugate journal · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide. The main etiologies of HCC are hepatitis B virus and hepatitis C virus (HCV), and non-hepatitis B/non-hepatitis C HCC (NBNC-HCC) has also been identified as an etiological factor. Although the incidence of HCV-related HCC in Japan has decreased slightly in recent years, that of NBNC-HCC has increased. The onset mechanism of NBNC-HCC, which has various etiologies, remains unclear; however, nonalcoholic steatohepatitis (NASH), a severe form of nonalcoholic fatty liver disease, is known to be an important risk factor for NBNC-HCC. Among the different advanced glycation end-products (AGEs) formed by the Maillard reaction, glyceraldehyde-derived AGEs, the predominant components of toxic AGEs (TAGE), have been associated with NASH and NBNC-HCC, including NASH-related HCC. Furthermore, the expression of the receptor for AGEs (RAGE) has been correlated with the malignant progression of HCC. Therefore, TAGE induce oxidative stress by binding with RAGE may, in turn, lead to adverse effects, such as fibrosis and malignant transformation, in hepatic stellate cells and tumor cells during NASH or NASH-related HCC progression. The aim of this review was to examine the contribution of the TAGE-RAGE axis in NASH-related HCC.
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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.