Next Article in Journal
GhMAP3K65, a Cotton Raf-Like MAP3K Gene, Enhances Susceptibility to Pathogen Infection and Heat Stress by Negatively Modulating Growth and Development in Transgenic Nicotiana benthamiana
Next Article in Special Issue
Probing Protein Glycation by Chromatography and Mass Spectrometry: Analysis of Glycation Adducts
Previous Article in Journal
Specific Effects of Chronic Dietary Exposure to Chlorpyrifos on Brain Gene Expression—A Mouse Study
Previous Article in Special Issue
Zebrafish as a Model for the Study of Microvascular Complications of Diabetes and Their Mechanisms
Article Menu
Issue 11 (November) cover image

Export Article

Open AccessReview
Int. J. Mol. Sci. 2017, 18(11), 2466;

The Role of Glyoxalase-I (Glo-I), Advanced Glycation Endproducts (AGEs), and Their Receptor (RAGE) in Chronic Liver Disease and Hepatocellular Carcinoma (HCC)

Department of Medicine, Neurology and Dermatology, Division of Gastroenterology and Rheumatology, University of Leipzig, Liebigstrasse 20, D-04103 Leipzig, Germany
Received: 31 October 2017 / Revised: 16 November 2017 / Accepted: 17 November 2017 / Published: 20 November 2017
(This article belongs to the Special Issue Glyoxalase System in Health and Disease 2017)
Full-Text   |   PDF [2894 KB, uploaded 20 November 2017]   |  


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. View Full-Text
Keywords: ethyl pyruvate; cirrhosis; fibrosis; methylglyoxal; AGEs; CCl4 ethyl pyruvate; cirrhosis; fibrosis; methylglyoxal; AGEs; CCl4

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

Share & Cite This Article

MDPI and ACS Style

Hollenbach, M. The Role of Glyoxalase-I (Glo-I), Advanced Glycation Endproducts (AGEs), and Their Receptor (RAGE) in Chronic Liver Disease and Hepatocellular Carcinoma (HCC). Int. J. Mol. Sci. 2017, 18, 2466.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top