RAGE is a Potential Cause of Onset and Progression of Nonalcoholic Fatty Liver Disease

Objective. Fatty liver is a rising global health concern, significantly increasing the burden of health care cost. Nonalcoholic fatty liver disease (NAFLD) has a correlation with metabolic syndrome and its complications. Method. We reviewed the literature regarding the mechanisms of developing NAFLD...

Full description

Saved in:
Bibliographic Details
Main Authors: Kamyar Asadipooya, Kamran B. Lankarani, Rishi Raj, Mohammadreza Kalantarhormozi
Format: Article
Language:English
Published: Wiley 2019-01-01
Series:International Journal of Endocrinology
Online Access:http://dx.doi.org/10.1155/2019/2151302
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1832567058872664064
author Kamyar Asadipooya
Kamran B. Lankarani
Rishi Raj
Mohammadreza Kalantarhormozi
author_facet Kamyar Asadipooya
Kamran B. Lankarani
Rishi Raj
Mohammadreza Kalantarhormozi
author_sort Kamyar Asadipooya
collection DOAJ
description Objective. Fatty liver is a rising global health concern, significantly increasing the burden of health care cost. Nonalcoholic fatty liver disease (NAFLD) has a correlation with metabolic syndrome and its complications. Method. We reviewed the literature regarding the mechanisms of developing NAFLD through AGE-RAGE signaling. Results. NAFLD, metabolic syndrome, and production of advanced glycation end-products (AGEs) share many common risk factors and appear to be connected. AGE induces production of the receptor for AGE (RAGE). AGE-RAGE interaction contributes to fat accumulation in the liver leading to inflammation, fibrosis, insulin resistance, and other complications of the fatty liver disease. The immune system, especially macrophages, has an important defense mechanism against RAGE pathway activities. Conclusion. Soluble form of RAGE (sRAGE) has the capability to reduce inflammation by blocking the interaction of AGE with RAGE. However, sRAGE has some limitations, and the best method of usage is probably autotransplantation of transfected stem cells or monocytes, as a precursor of macrophages and Kupffer cells, with a virus that carries sRAGE to alleviate the harmful effects of AGE-RAGE signaling in the settings of fatty liver disease.
format Article
id doaj-art-c51117f35a0343b6888d9527ad40483e
institution Kabale University
issn 1687-8337
1687-8345
language English
publishDate 2019-01-01
publisher Wiley
record_format Article
series International Journal of Endocrinology
spelling doaj-art-c51117f35a0343b6888d9527ad40483e2025-02-03T01:02:29ZengWileyInternational Journal of Endocrinology1687-83371687-83452019-01-01201910.1155/2019/21513022151302RAGE is a Potential Cause of Onset and Progression of Nonalcoholic Fatty Liver DiseaseKamyar Asadipooya0Kamran B. Lankarani1Rishi Raj2Mohammadreza Kalantarhormozi3Division of Endocrinology and Molecular Medicine, Department of Medicine, University of Kentucky, Lexington, KY, USAHealth Policy Research Center, Institute of Health, Shiraz University of Medical Sciences, Shiraz, IranDivision of Endocrinology and Molecular Medicine, Department of Medicine, University of Kentucky, Lexington, KY, USAEndocrinology and Internal Medicine, The Persian Gulf Tropical Medicine Research Center, Bushehr University of Medical Sciences, Bushehr, IranObjective. Fatty liver is a rising global health concern, significantly increasing the burden of health care cost. Nonalcoholic fatty liver disease (NAFLD) has a correlation with metabolic syndrome and its complications. Method. We reviewed the literature regarding the mechanisms of developing NAFLD through AGE-RAGE signaling. Results. NAFLD, metabolic syndrome, and production of advanced glycation end-products (AGEs) share many common risk factors and appear to be connected. AGE induces production of the receptor for AGE (RAGE). AGE-RAGE interaction contributes to fat accumulation in the liver leading to inflammation, fibrosis, insulin resistance, and other complications of the fatty liver disease. The immune system, especially macrophages, has an important defense mechanism against RAGE pathway activities. Conclusion. Soluble form of RAGE (sRAGE) has the capability to reduce inflammation by blocking the interaction of AGE with RAGE. However, sRAGE has some limitations, and the best method of usage is probably autotransplantation of transfected stem cells or monocytes, as a precursor of macrophages and Kupffer cells, with a virus that carries sRAGE to alleviate the harmful effects of AGE-RAGE signaling in the settings of fatty liver disease.http://dx.doi.org/10.1155/2019/2151302
spellingShingle Kamyar Asadipooya
Kamran B. Lankarani
Rishi Raj
Mohammadreza Kalantarhormozi
RAGE is a Potential Cause of Onset and Progression of Nonalcoholic Fatty Liver Disease
International Journal of Endocrinology
title RAGE is a Potential Cause of Onset and Progression of Nonalcoholic Fatty Liver Disease
title_full RAGE is a Potential Cause of Onset and Progression of Nonalcoholic Fatty Liver Disease
title_fullStr RAGE is a Potential Cause of Onset and Progression of Nonalcoholic Fatty Liver Disease
title_full_unstemmed RAGE is a Potential Cause of Onset and Progression of Nonalcoholic Fatty Liver Disease
title_short RAGE is a Potential Cause of Onset and Progression of Nonalcoholic Fatty Liver Disease
title_sort rage is a potential cause of onset and progression of nonalcoholic fatty liver disease
url http://dx.doi.org/10.1155/2019/2151302
work_keys_str_mv AT kamyarasadipooya rageisapotentialcauseofonsetandprogressionofnonalcoholicfattyliverdisease
AT kamranblankarani rageisapotentialcauseofonsetandprogressionofnonalcoholicfattyliverdisease
AT rishiraj rageisapotentialcauseofonsetandprogressionofnonalcoholicfattyliverdisease
AT mohammadrezakalantarhormozi rageisapotentialcauseofonsetandprogressionofnonalcoholicfattyliverdisease