Loading…
The Role of Advanced Glycation End Products and Its Soluble Receptor in Kidney Diseases
Patients with chronic kidney disease (CKD) are more prone to oxidative stress and chronic inflammation, which may lead to an increase in the synthesis of advanced glycation end products (AGEs). Because AGEs are mostly removed by healthy kidneys, AGE accumulation is a result of both increased product...
Saved in:
Published in: | International journal of molecular sciences 2022-03, Vol.23 (7), p.3439 |
---|---|
Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
cited_by | cdi_FETCH-LOGICAL-c478t-6f672b4c7942286762bd2b9240b963e6ff824ef2e7edbfa41b7fcbb21c053c753 |
---|---|
cites | cdi_FETCH-LOGICAL-c478t-6f672b4c7942286762bd2b9240b963e6ff824ef2e7edbfa41b7fcbb21c053c753 |
container_end_page | |
container_issue | 7 |
container_start_page | 3439 |
container_title | International journal of molecular sciences |
container_volume | 23 |
creator | Steenbeke, Mieke Speeckaert, Reinhart Desmedt, Stéphanie Glorieux, Griet Delanghe, Joris R Speeckaert, Marijn M |
description | Patients with chronic kidney disease (CKD) are more prone to oxidative stress and chronic inflammation, which may lead to an increase in the synthesis of advanced glycation end products (AGEs). Because AGEs are mostly removed by healthy kidneys, AGE accumulation is a result of both increased production and decreased kidney clearance. On the other hand, AGEs may potentially hasten decreasing kidney function in CKD patients, and are independently related to all-cause mortality. They are one of the non-traditional risk factors that play a significant role in the underlying processes that lead to excessive cardiovascular disease in CKD patients. When AGEs interact with their cell-bound receptor (RAGE), cell dysfunction is initiated by activating nuclear factor kappa-B (NF-κB), increasing the production and release of inflammatory cytokines. Alterations in the AGE-RAGE system have been related to the development of several chronic kidney diseases. Soluble RAGE (sRAGE) is a decoy receptor that suppresses membrane-bound RAGE activation and AGE-RAGE-related toxicity. sRAGE, and more specifically, the AGE/sRAGE ratio, may be promising tools for predicting the prognosis of kidney diseases. In the present review, we discuss the potential role of AGEs and sRAGE as biomarkers in different kidney pathologies. |
doi_str_mv | 10.3390/ijms23073439 |
format | article |
fullrecord | <record><control><sourceid>proquest_doaj_</sourceid><recordid>TN_cdi_doaj_primary_oai_doaj_org_article_4a25514526d64fdc9927fbfa3798991f</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><doaj_id>oai_doaj_org_article_4a25514526d64fdc9927fbfa3798991f</doaj_id><sourcerecordid>2649057453</sourcerecordid><originalsourceid>FETCH-LOGICAL-c478t-6f672b4c7942286762bd2b9240b963e6ff824ef2e7edbfa41b7fcbb21c053c753</originalsourceid><addsrcrecordid>eNpdkctPVDEUh2-MRhDduTZN3LhwoLfP240JQYSJJBrEuGz6OIVO7twO7b0k899bZoAMrE4f3_ly2l_TfGzxIaUKH8XFshCKJWVUvWr2W0bIDGMhX--s95p3pSwwJpRw9bbZo5zhTiqx3_y7ugF0mXpAKaBjf2cGBx6d9WtnxpgGdDp49DsnP7mxIFM381r_pH6yteUSHKzGlFEc0M_oB1ij77GAKVDeN2-C6Qt8eKgHzd8fp1cn57OLX2fzk-OLmWOyG2ciCEksc1LVUTshBbGeWEUYtkpQECF0hEEgIMHbYFhrZXDWktZhTp3k9KCZb70-mYVe5bg0ea2TiXpzkPK1NnmMrgfNDOG8ZZwIL1jwTikiQ5VSqTql2lBd37au1WSX4B0MYzb9M-nzmyHe6Ot0p2t7122G-fIgyOl2gjLqZSwO-t4MkKaiiWCKd4oLUdHPL9BFmvJQv2pDYS4Zp5X6uqVcTqVkCE_DtFjfp69306_4p90HPMGPcdP_ZwqqRg</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2649057453</pqid></control><display><type>article</type><title>The Role of Advanced Glycation End Products and Its Soluble Receptor in Kidney Diseases</title><source>Publicly Available Content Database</source><source>PubMed Central</source><creator>Steenbeke, Mieke ; Speeckaert, Reinhart ; Desmedt, Stéphanie ; Glorieux, Griet ; Delanghe, Joris R ; Speeckaert, Marijn M</creator><creatorcontrib>Steenbeke, Mieke ; Speeckaert, Reinhart ; Desmedt, Stéphanie ; Glorieux, Griet ; Delanghe, Joris R ; Speeckaert, Marijn M</creatorcontrib><description>Patients with chronic kidney disease (CKD) are more prone to oxidative stress and chronic inflammation, which may lead to an increase in the synthesis of advanced glycation end products (AGEs). Because AGEs are mostly removed by healthy kidneys, AGE accumulation is a result of both increased production and decreased kidney clearance. On the other hand, AGEs may potentially hasten decreasing kidney function in CKD patients, and are independently related to all-cause mortality. They are one of the non-traditional risk factors that play a significant role in the underlying processes that lead to excessive cardiovascular disease in CKD patients. When AGEs interact with their cell-bound receptor (RAGE), cell dysfunction is initiated by activating nuclear factor kappa-B (NF-κB), increasing the production and release of inflammatory cytokines. Alterations in the AGE-RAGE system have been related to the development of several chronic kidney diseases. Soluble RAGE (sRAGE) is a decoy receptor that suppresses membrane-bound RAGE activation and AGE-RAGE-related toxicity. sRAGE, and more specifically, the AGE/sRAGE ratio, may be promising tools for predicting the prognosis of kidney diseases. In the present review, we discuss the potential role of AGEs and sRAGE as biomarkers in different kidney pathologies.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms23073439</identifier><identifier>PMID: 35408796</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>advanced glycation end products (AGEs) ; Advanced glycosylation end products ; Age ; Binding sites ; Biomarkers ; Body mass index ; Cardiovascular Diseases ; Chromatography ; Chronic illnesses ; chronic kidney disease (CKD) ; Cytokines ; Diabetes ; Glycation End Products, Advanced ; Glycosylation ; Humans ; Inflammation ; Kidney diseases ; Kinases ; Ligands ; NF-κB protein ; Oxidative stress ; Proteins ; Receptor for Advanced Glycation End Products ; Renal Insufficiency, Chronic ; Review ; Risk analysis ; Risk factors ; Skin ; soluble receptor for AGEs (sRAGE) ; Toxicity ; Tumor necrosis factor-TNF ; Uremia</subject><ispartof>International journal of molecular sciences, 2022-03, Vol.23 (7), p.3439</ispartof><rights>2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2022 by the authors. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c478t-6f672b4c7942286762bd2b9240b963e6ff824ef2e7edbfa41b7fcbb21c053c753</citedby><cites>FETCH-LOGICAL-c478t-6f672b4c7942286762bd2b9240b963e6ff824ef2e7edbfa41b7fcbb21c053c753</cites><orcidid>0000-0003-2731-7545 ; 0000-0002-6846-6558 ; 0000-0002-5702-6792 ; 0000-0001-9183-4390 ; 0000-0002-7641-4707</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2649057453/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2649057453?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35408796$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Steenbeke, Mieke</creatorcontrib><creatorcontrib>Speeckaert, Reinhart</creatorcontrib><creatorcontrib>Desmedt, Stéphanie</creatorcontrib><creatorcontrib>Glorieux, Griet</creatorcontrib><creatorcontrib>Delanghe, Joris R</creatorcontrib><creatorcontrib>Speeckaert, Marijn M</creatorcontrib><title>The Role of Advanced Glycation End Products and Its Soluble Receptor in Kidney Diseases</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>Patients with chronic kidney disease (CKD) are more prone to oxidative stress and chronic inflammation, which may lead to an increase in the synthesis of advanced glycation end products (AGEs). Because AGEs are mostly removed by healthy kidneys, AGE accumulation is a result of both increased production and decreased kidney clearance. On the other hand, AGEs may potentially hasten decreasing kidney function in CKD patients, and are independently related to all-cause mortality. They are one of the non-traditional risk factors that play a significant role in the underlying processes that lead to excessive cardiovascular disease in CKD patients. When AGEs interact with their cell-bound receptor (RAGE), cell dysfunction is initiated by activating nuclear factor kappa-B (NF-κB), increasing the production and release of inflammatory cytokines. Alterations in the AGE-RAGE system have been related to the development of several chronic kidney diseases. Soluble RAGE (sRAGE) is a decoy receptor that suppresses membrane-bound RAGE activation and AGE-RAGE-related toxicity. sRAGE, and more specifically, the AGE/sRAGE ratio, may be promising tools for predicting the prognosis of kidney diseases. In the present review, we discuss the potential role of AGEs and sRAGE as biomarkers in different kidney pathologies.</description><subject>advanced glycation end products (AGEs)</subject><subject>Advanced glycosylation end products</subject><subject>Age</subject><subject>Binding sites</subject><subject>Biomarkers</subject><subject>Body mass index</subject><subject>Cardiovascular Diseases</subject><subject>Chromatography</subject><subject>Chronic illnesses</subject><subject>chronic kidney disease (CKD)</subject><subject>Cytokines</subject><subject>Diabetes</subject><subject>Glycation End Products, Advanced</subject><subject>Glycosylation</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Kidney diseases</subject><subject>Kinases</subject><subject>Ligands</subject><subject>NF-κB protein</subject><subject>Oxidative stress</subject><subject>Proteins</subject><subject>Receptor for Advanced Glycation End Products</subject><subject>Renal Insufficiency, Chronic</subject><subject>Review</subject><subject>Risk analysis</subject><subject>Risk factors</subject><subject>Skin</subject><subject>soluble receptor for AGEs (sRAGE)</subject><subject>Toxicity</subject><subject>Tumor necrosis factor-TNF</subject><subject>Uremia</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNpdkctPVDEUh2-MRhDduTZN3LhwoLfP240JQYSJJBrEuGz6OIVO7twO7b0k899bZoAMrE4f3_ly2l_TfGzxIaUKH8XFshCKJWVUvWr2W0bIDGMhX--s95p3pSwwJpRw9bbZo5zhTiqx3_y7ugF0mXpAKaBjf2cGBx6d9WtnxpgGdDp49DsnP7mxIFM381r_pH6yteUSHKzGlFEc0M_oB1ij77GAKVDeN2-C6Qt8eKgHzd8fp1cn57OLX2fzk-OLmWOyG2ciCEksc1LVUTshBbGeWEUYtkpQECF0hEEgIMHbYFhrZXDWktZhTp3k9KCZb70-mYVe5bg0ea2TiXpzkPK1NnmMrgfNDOG8ZZwIL1jwTikiQ5VSqTql2lBd37au1WSX4B0MYzb9M-nzmyHe6Ot0p2t7122G-fIgyOl2gjLqZSwO-t4MkKaiiWCKd4oLUdHPL9BFmvJQv2pDYS4Zp5X6uqVcTqVkCE_DtFjfp69306_4p90HPMGPcdP_ZwqqRg</recordid><startdate>20220322</startdate><enddate>20220322</enddate><creator>Steenbeke, Mieke</creator><creator>Speeckaert, Reinhart</creator><creator>Desmedt, Stéphanie</creator><creator>Glorieux, Griet</creator><creator>Delanghe, Joris R</creator><creator>Speeckaert, Marijn M</creator><general>MDPI AG</general><general>MDPI</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0003-2731-7545</orcidid><orcidid>https://orcid.org/0000-0002-6846-6558</orcidid><orcidid>https://orcid.org/0000-0002-5702-6792</orcidid><orcidid>https://orcid.org/0000-0001-9183-4390</orcidid><orcidid>https://orcid.org/0000-0002-7641-4707</orcidid></search><sort><creationdate>20220322</creationdate><title>The Role of Advanced Glycation End Products and Its Soluble Receptor in Kidney Diseases</title><author>Steenbeke, Mieke ; Speeckaert, Reinhart ; Desmedt, Stéphanie ; Glorieux, Griet ; Delanghe, Joris R ; Speeckaert, Marijn M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c478t-6f672b4c7942286762bd2b9240b963e6ff824ef2e7edbfa41b7fcbb21c053c753</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>advanced glycation end products (AGEs)</topic><topic>Advanced glycosylation end products</topic><topic>Age</topic><topic>Binding sites</topic><topic>Biomarkers</topic><topic>Body mass index</topic><topic>Cardiovascular Diseases</topic><topic>Chromatography</topic><topic>Chronic illnesses</topic><topic>chronic kidney disease (CKD)</topic><topic>Cytokines</topic><topic>Diabetes</topic><topic>Glycation End Products, Advanced</topic><topic>Glycosylation</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Kidney diseases</topic><topic>Kinases</topic><topic>Ligands</topic><topic>NF-κB protein</topic><topic>Oxidative stress</topic><topic>Proteins</topic><topic>Receptor for Advanced Glycation End Products</topic><topic>Renal Insufficiency, Chronic</topic><topic>Review</topic><topic>Risk analysis</topic><topic>Risk factors</topic><topic>Skin</topic><topic>soluble receptor for AGEs (sRAGE)</topic><topic>Toxicity</topic><topic>Tumor necrosis factor-TNF</topic><topic>Uremia</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Steenbeke, Mieke</creatorcontrib><creatorcontrib>Speeckaert, Reinhart</creatorcontrib><creatorcontrib>Desmedt, Stéphanie</creatorcontrib><creatorcontrib>Glorieux, Griet</creatorcontrib><creatorcontrib>Delanghe, Joris R</creatorcontrib><creatorcontrib>Speeckaert, Marijn M</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Steenbeke, Mieke</au><au>Speeckaert, Reinhart</au><au>Desmedt, Stéphanie</au><au>Glorieux, Griet</au><au>Delanghe, Joris R</au><au>Speeckaert, Marijn M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Role of Advanced Glycation End Products and Its Soluble Receptor in Kidney Diseases</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2022-03-22</date><risdate>2022</risdate><volume>23</volume><issue>7</issue><spage>3439</spage><pages>3439-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>Patients with chronic kidney disease (CKD) are more prone to oxidative stress and chronic inflammation, which may lead to an increase in the synthesis of advanced glycation end products (AGEs). Because AGEs are mostly removed by healthy kidneys, AGE accumulation is a result of both increased production and decreased kidney clearance. On the other hand, AGEs may potentially hasten decreasing kidney function in CKD patients, and are independently related to all-cause mortality. They are one of the non-traditional risk factors that play a significant role in the underlying processes that lead to excessive cardiovascular disease in CKD patients. When AGEs interact with their cell-bound receptor (RAGE), cell dysfunction is initiated by activating nuclear factor kappa-B (NF-κB), increasing the production and release of inflammatory cytokines. Alterations in the AGE-RAGE system have been related to the development of several chronic kidney diseases. Soluble RAGE (sRAGE) is a decoy receptor that suppresses membrane-bound RAGE activation and AGE-RAGE-related toxicity. sRAGE, and more specifically, the AGE/sRAGE ratio, may be promising tools for predicting the prognosis of kidney diseases. In the present review, we discuss the potential role of AGEs and sRAGE as biomarkers in different kidney pathologies.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>35408796</pmid><doi>10.3390/ijms23073439</doi><orcidid>https://orcid.org/0000-0003-2731-7545</orcidid><orcidid>https://orcid.org/0000-0002-6846-6558</orcidid><orcidid>https://orcid.org/0000-0002-5702-6792</orcidid><orcidid>https://orcid.org/0000-0001-9183-4390</orcidid><orcidid>https://orcid.org/0000-0002-7641-4707</orcidid><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 1422-0067 |
ispartof | International journal of molecular sciences, 2022-03, Vol.23 (7), p.3439 |
issn | 1422-0067 1661-6596 1422-0067 |
language | eng |
recordid | cdi_doaj_primary_oai_doaj_org_article_4a25514526d64fdc9927fbfa3798991f |
source | Publicly Available Content Database; PubMed Central |
subjects | advanced glycation end products (AGEs) Advanced glycosylation end products Age Binding sites Biomarkers Body mass index Cardiovascular Diseases Chromatography Chronic illnesses chronic kidney disease (CKD) Cytokines Diabetes Glycation End Products, Advanced Glycosylation Humans Inflammation Kidney diseases Kinases Ligands NF-κB protein Oxidative stress Proteins Receptor for Advanced Glycation End Products Renal Insufficiency, Chronic Review Risk analysis Risk factors Skin soluble receptor for AGEs (sRAGE) Toxicity Tumor necrosis factor-TNF Uremia |
title | The Role of Advanced Glycation End Products and Its Soluble Receptor in Kidney Diseases |
url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-01T03%3A20%3A26IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_doaj_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=The%20Role%20of%20Advanced%20Glycation%20End%20Products%20and%20Its%20Soluble%20Receptor%20in%20Kidney%20Diseases&rft.jtitle=International%20journal%20of%20molecular%20sciences&rft.au=Steenbeke,%20Mieke&rft.date=2022-03-22&rft.volume=23&rft.issue=7&rft.spage=3439&rft.pages=3439-&rft.issn=1422-0067&rft.eissn=1422-0067&rft_id=info:doi/10.3390/ijms23073439&rft_dat=%3Cproquest_doaj_%3E2649057453%3C/proquest_doaj_%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c478t-6f672b4c7942286762bd2b9240b963e6ff824ef2e7edbfa41b7fcbb21c053c753%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=2649057453&rft_id=info:pmid/35408796&rfr_iscdi=true |