ReviewEuropean journal of medical research2015
Role of receptor for advanced glycation end products (RAGE) in liver disease.
Review in European journal of medical research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 73 citations in OpenAlex.
- Association Between Dietary Advanced Glycation End Products (AGEs) and Pancreatic Fat Accumulation: Evidence From a Case-Control Study.Endocrinology, diabetes & metabolism · 2026Article
- AGE-RAGE Axis Involvement in Allergies and Autoimmunity: Cellular Signaling, Barrier Dysfunction and Immune Polarization.Biomolecules · 2026Review
- Quantifying interventional causality by knockoff operation.Science advances · 2025Article
- Comparative Effects of Crocin and Losartan on RAGE, TGF-β, TNF-α Gene Expression and Histopathological Changes of the Liver Tissue in Rats With Diabetes.Endocrinology, diabetes & metabolism · 2025Article
- 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
- Emerging Roles of High-mobility Group Box-1 in Liver Disease.Journal of clinical and translational hepatology · 2024Review
- Deletion of Glyoxalase 1 Exacerbates Acetaminophen-Induced Hepatotoxicity in Mice.Antioxidants (Basel, Switzerland) · 2024Article
- Metabolic memory: mechanisms and diseases.Signal transduction and targeted therapy · 2024Review
- Deletion of Glyoxalase 1 exacerbates acetaminophen-induced hepatotoxicity in mice.bioRxiv : the preprint server for biology · 2023Article
- Association between hemoglobin glycation index and non-alcoholic fatty liver disease in the patients with type 2 diabetes mellitus.Journal of diabetes investigation · 2023Article
- Profile analysis of differentially expressed long non‑coding RNAs in metabolic memory induced by high glucose in human umbilical vein endothelial cells.Experimental and therapeutic medicine · 2023Article
- Alcohol as a Modifiable Risk Factor for Alzheimer's Disease-Evidence from Experimental Studies.International journal of molecular sciences · 2023Review
- SMTP-44D Inhibits Atherosclerotic Plaque Formation in Apolipoprotein-E Null Mice Partly by Suppressing the AGEs-RAGE Axis.International journal of molecular sciences · 2023Article
- Aging-Accelerated Mouse Prone 8 (SAMP8) Mice Experiment and Network Pharmacological Analysis of Aged Liupao Tea Aqueous Extract in Delaying the Decline Changes of the Body.Antioxidants (Basel, Switzerland) · 2023Article
- A standardized pomegranate fruit extract ameliorates thioacetamide-induced liver fibrosis in rats via AGE-RAGE-ROS signaling.Heliyon · 2023Article
- Soluble receptors for advanced glycation end-products prevent unilateral ureteral obstruction-induced renal fibrosis.Frontiers in pharmacology · 2023Article
- Targeting the liver in dementia and cognitive impairment: Dietary macronutrients and diabetic therapeutics.Advanced drug delivery reviews · 2022Review
- Systems pharmacology dissection of the mechanisms and therapeutic potential of Cassiae semen for hepatoprotection and brightening eyes.Journal of food and drug analysis · 2022Article
- Deriving time-concordant event cascades from gene expression data: A case study for Drug-Induced Liver Injury (DILI).PLoS computational biology · 2022Article
- From Inflammation to Fibrosis: Novel Insights into the Roles of High Mobility Group Protein Box 1 in Schistosome-Induced Liver Damage.Pathogens (Basel, Switzerland) · 2022Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Receptor for advanced glycation end products (RAGE) belongs to a immunoglobulin superfamily of cell surface molecules that could bind to a number of ligands such as advanced glycation end products, high-mobility group protein box-1, S-100 calcium-binding protein, and amyloid-β-protein, inducing a series of signal transduction cascades, and being involved in a variety of cellular function, including inflammation, proliferation, apoptosis, angiogenesis, migration, and fibrosis. RAGE is expressed in hepatic stellate cells and hepatocytes and hepatoma cells. There is accumulating evidence that engagement of RAGE with various ligands elicits oxidative stress generation and subsequently activates the RAGE downstream pathway in the liver, thereby contributing to the development and progression of numerous types of hepatic disorders. These observations suggest that inhibition of the RAGE signaling pathway could be a novel therapeutic target for liver diseases. This article summarizes the pathological role of RAGE in hepatic insulin resistance, steatosis and fibrosis, ischemic and non-ischemic liver injury, and hepatocellular carcinoma growth and metastasis and its therapeutic interventions for these devastating disorders.
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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.