ArticlePloS one2018
Polymorphisms in the receptor for advanced glycation end-products (RAGE) gene and circulating RAGE levels as a susceptibility factor for non-alcoholic steatohepatitis (NASH).
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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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.
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- Advanced Glycation End-Products in Common Non-Infectious Liver Diseases: Systematic Review and Meta-Analysis.Nutrients · 2021Pooled it
- Serum-Soluble Receptor for Advanced Glycation End Products as a Potential Biomarker in Lung Cancer Patients.Journal of personalized medicine · 2026Article
- Current Developments in Analytical Methods for Advanced Glycation End Products in Foods.Molecules (Basel, Switzerland) · 2025Review
- Is There a Diagnostic Miracle on the Horizon? Emerging Biomarkers in MASLD.Journal of clinical medicine · 2025Review
- Advanced Glycation End Products in Disease Development and Potential Interventions.Antioxidants (Basel, Switzerland) · 2025Review
- Construction and evaluation of a diagnostic model for metabolic dysfunction-associated steatotic liver disease based on advanced glycation end products and their receptors.Frontiers in medicine · 2025Article
- The contribution of adiponectin to diabetic retinopathy progression: Association with the AGEs-RAGE pathway.Heliyon · 2024Article
- RAGE engagement by SARS-CoV-2 enables monocyte infection and underlies COVID-19 severity.Cell reports. Medicine · 2023Article
- Article
- Association between hemoglobin glycation index and non-alcoholic fatty liver disease.Frontiers in endocrinology · 2023Article
- Association between plasma sRAGE and emphysema according to the genotypes of AGER gene.BMC pulmonary medicine · 2022Article
- Single nucleotide variants of receptor for advanced glycation end-products (AGER) gene: is it a new opening in the risk assessment of diabetic retinopathy?-a review.Journal, genetic engineering & biotechnology · 2022Review
- Danger signals in liver injury and restoration of homeostasis.Journal of hepatology · 2020Review
- HbA1c may contribute to the development of non-alcoholic fatty liver disease even at normal-range levels.Bioscience reports · 2020Article
- Indole-4-carboxaldehyde Isolated from Seaweed,Marine drugs · 2019Article
- Association between Hemoglobin Glycation Index and NAFLD in Chinese Nondiabetic Individuals.Canadian journal of gastroenterology & hepatology · 2019Article
- RAGE is a Potential Cause of Onset and Progression of Nonalcoholic Fatty Liver Disease.International journal of endocrinology · 2019Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Non-alcoholic fatty liver disease (NAFLD) is a hepatic manifestation of metabolic syndrome and major cause of chronic liver disease in developed countries. Its prevalence is increasing in parallel with the prevalence of obesity and other components of the metabolic syndrome. As the liver is central to the clearance and catabolism of circulating advanced glycosylation end-products (AGEs), AGEs and their cognate receptors-RAGE (receptor for AGEs) system might be involved in NAFLD in obese patients. To examine this, we investigated four common polymorphisms of RAGE gene: 1704G/T (rs184003), G82S (rs2070600), -374T/A (rs1800624) and -429T/C (rs1800625) in 340 obese patients with metabolic syndrome. and protein levels of AGE and RAGE. This is the first study to describe association of 4 common polymorphisms with non-alcoholic steatohepatitis (NASH) as well as to examine protein levels of RAGE and AGE. Univariate analysis showed patients carrying the rs1800624 heterozygote genotype (AT) exhibited 2.36-fold increased risk of NASH (odds ratio (OR) = 2.36; 95% confidence interval (95% CI): 1.35-4.19) after adjusting for confounders. The minor allele -374 A has been shown to suppress the expression of RAGE protein. The protein levels of esRAGE, total sRAGE and AGE protein levels did not correlate with each other in obese patients with no liver disease, indicative of RAGE signaling playing an independent role in liver injury. In obese patients with non-NASH NAFLD and NASH respectively, esRAGE protein showed strong positive correlation with total sRAGE protein. Further, haplotype analysis of the 4 SNPs, indicated that haplotype G-A-T-G was significantly associated with 2-fold increased risk for NASH (OR = 2.08; 95% CI: 1.21-3.5; P = 0.006) after adjusting for confounders. In conclusion, the presented data indicate that the G-A-T-G haplotype containing minor allele at position -374 A and major allele at position -429T, 1704G, and G82S G could be regarded as a marker for NASH.
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