Activation of receptor for advanced glycation end products contributes to aortic remodeling and endothelial dysfunction in sinoaortic denervated rats
Abstract Objective The aim of present study was to test the hypothesis that activation of receptor for advanced glycation end products (RAGE) pathway contributes to aortic remodeling and endothelial dysfunction in sinoaortic denervated (SAD) rats. Methods and results Experiment 1 : 8 weeks after sin...
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| Veröffentlicht in: | Atherosclerosis 2013-08, Vol.229 (2), p.287-294 |
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| creator | Wu, Feng Feng, Jin-Zhong Qiu, Yi-Hua Yu, Feng-Bin Zhang, Jian-Zhong Zhou, Wei Yu, Feng Wang, Guo-Kun An, Li-Na Ni, Fei-Hua Wu, Hong Zhao, Xian-Xian Qin, Yong-Wen Luo, He-De |
| description | Abstract Objective The aim of present study was to test the hypothesis that activation of receptor for advanced glycation end products (RAGE) pathway contributes to aortic remodeling and endothelial dysfunction in sinoaortic denervated (SAD) rats. Methods and results Experiment 1 : 8 weeks after sinoaortic denervation, aortas were removed for measurement of AGE/RAGE pathway. Sinoaortic denervation in rats resulted in enhanced activity of aldose reductase, reduced activity of glyoxalase 1, accumulation of methylglyoxal and AGE, and upregulated expression of RAGE in aortas. Experiment 2 : 5 weeks after sinoaortic denervation, the rats received intraperitoneal injections of 500 μg soluble RAGE (sRAGE) daily for 3 weeks. Treatment of SAD rats with sRAGE attenuated aortic remodeling, marked by reduction in AW/length, wall thickness, proliferation of SMC, and collagen deposition, and improvement of endothelial function. Treatment of SAD rats with sRAGE abated aortic oxidative stress, marked by reduction in formation of malondialdehyde, reactive oxygen species, superoxide, peroxynitrite and 3-nitrotyrosine, and enhancement of ratio of GSH/GSSG. Treatment of SAD rats with sRAGE attenuated aortic mitochondrial dysfunction. Treatment of SAD rats with sRAGE suppressed aortic NFκB nuclear translocation and inflammation. Treatment of SAD rats with sRAGE restored aortic NO formation through upregulating eNOS and dimethylarginine dimethylaminohydrolase-2 and downregulating protein arginine methyltransferase-1. Conclusion Activated RAGE contributed to aortic remodeling and endothelial dysfunction in SAD rats, possibly via induction of oxidative stress and inflammation, impairment of mitochondrial function, and reduction in NO bioavailability. |
| doi_str_mv | 10.1016/j.atherosclerosis.2013.04.033 |
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Methods and results Experiment 1 : 8 weeks after sinoaortic denervation, aortas were removed for measurement of AGE/RAGE pathway. Sinoaortic denervation in rats resulted in enhanced activity of aldose reductase, reduced activity of glyoxalase 1, accumulation of methylglyoxal and AGE, and upregulated expression of RAGE in aortas. Experiment 2 : 5 weeks after sinoaortic denervation, the rats received intraperitoneal injections of 500 μg soluble RAGE (sRAGE) daily for 3 weeks. Treatment of SAD rats with sRAGE attenuated aortic remodeling, marked by reduction in AW/length, wall thickness, proliferation of SMC, and collagen deposition, and improvement of endothelial function. Treatment of SAD rats with sRAGE abated aortic oxidative stress, marked by reduction in formation of malondialdehyde, reactive oxygen species, superoxide, peroxynitrite and 3-nitrotyrosine, and enhancement of ratio of GSH/GSSG. Treatment of SAD rats with sRAGE attenuated aortic mitochondrial dysfunction. Treatment of SAD rats with sRAGE suppressed aortic NFκB nuclear translocation and inflammation. Treatment of SAD rats with sRAGE restored aortic NO formation through upregulating eNOS and dimethylarginine dimethylaminohydrolase-2 and downregulating protein arginine methyltransferase-1. Conclusion Activated RAGE contributed to aortic remodeling and endothelial dysfunction in SAD rats, possibly via induction of oxidative stress and inflammation, impairment of mitochondrial function, and reduction in NO bioavailability.</description><identifier>ISSN: 0021-9150</identifier><identifier>EISSN: 1879-1484</identifier><identifier>DOI: 10.1016/j.atherosclerosis.2013.04.033</identifier><identifier>PMID: 23880178</identifier><language>eng</language><publisher>Ireland: Elsevier Ireland Ltd</publisher><subject>advanced glycation end products ; aldehyde reductase ; Aldehyde Reductase - metabolism ; Animals ; Aorta - innervation ; Aorta - metabolism ; Aorta - physiopathology ; Aortic remodeling ; arginine ; atherosclerosis ; Autonomic Denervation ; Baroreflex - physiology ; bioavailability ; Cardiovascular ; Cardiovascular Diseases - metabolism ; Cardiovascular Diseases - physiopathology ; collagen ; Disease Models, Animal ; Endothelial dysfunction ; endothelial nitric oxide synthase ; Endothelium, Vascular - innervation ; Endothelium, Vascular - metabolism ; Endothelium, Vascular - physiopathology ; Inflammation ; Lactoylglutathione Lyase - metabolism ; Male ; malondialdehyde ; Mitochondria - metabolism ; Nitric oxide ; Nitric Oxide - metabolism ; Nitric Oxide Synthase Type III - metabolism ; Oxidative stress ; Oxidative Stress - physiology ; Rats ; Rats, Sprague-Dawley ; reactive oxygen species ; Receptor for Advanced Glycation End Products ; Receptors, Immunologic - metabolism ; Sinoaortic denervation ; Vasculitis - metabolism ; Vasculitis - physiopathology</subject><ispartof>Atherosclerosis, 2013-08, Vol.229 (2), p.287-294</ispartof><rights>Elsevier Ireland Ltd</rights><rights>2013 Elsevier Ireland Ltd</rights><rights>Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c589t-fe3bb4168e30b7386812db23fa311170ab661d9da83a4e6a21259dbd5a5f8b9e3</citedby><cites>FETCH-LOGICAL-c589t-fe3bb4168e30b7386812db23fa311170ab661d9da83a4e6a21259dbd5a5f8b9e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S002191501300275X$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23880178$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wu, Feng</creatorcontrib><creatorcontrib>Feng, Jin-Zhong</creatorcontrib><creatorcontrib>Qiu, Yi-Hua</creatorcontrib><creatorcontrib>Yu, Feng-Bin</creatorcontrib><creatorcontrib>Zhang, Jian-Zhong</creatorcontrib><creatorcontrib>Zhou, Wei</creatorcontrib><creatorcontrib>Yu, Feng</creatorcontrib><creatorcontrib>Wang, Guo-Kun</creatorcontrib><creatorcontrib>An, Li-Na</creatorcontrib><creatorcontrib>Ni, Fei-Hua</creatorcontrib><creatorcontrib>Wu, Hong</creatorcontrib><creatorcontrib>Zhao, Xian-Xian</creatorcontrib><creatorcontrib>Qin, Yong-Wen</creatorcontrib><creatorcontrib>Luo, He-De</creatorcontrib><title>Activation of receptor for advanced glycation end products contributes to aortic remodeling and endothelial dysfunction in sinoaortic denervated rats</title><title>Atherosclerosis</title><addtitle>Atherosclerosis</addtitle><description>Abstract Objective The aim of present study was to test the hypothesis that activation of receptor for advanced glycation end products (RAGE) pathway contributes to aortic remodeling and endothelial dysfunction in sinoaortic denervated (SAD) rats. Methods and results Experiment 1 : 8 weeks after sinoaortic denervation, aortas were removed for measurement of AGE/RAGE pathway. Sinoaortic denervation in rats resulted in enhanced activity of aldose reductase, reduced activity of glyoxalase 1, accumulation of methylglyoxal and AGE, and upregulated expression of RAGE in aortas. Experiment 2 : 5 weeks after sinoaortic denervation, the rats received intraperitoneal injections of 500 μg soluble RAGE (sRAGE) daily for 3 weeks. Treatment of SAD rats with sRAGE attenuated aortic remodeling, marked by reduction in AW/length, wall thickness, proliferation of SMC, and collagen deposition, and improvement of endothelial function. Treatment of SAD rats with sRAGE abated aortic oxidative stress, marked by reduction in formation of malondialdehyde, reactive oxygen species, superoxide, peroxynitrite and 3-nitrotyrosine, and enhancement of ratio of GSH/GSSG. Treatment of SAD rats with sRAGE attenuated aortic mitochondrial dysfunction. Treatment of SAD rats with sRAGE suppressed aortic NFκB nuclear translocation and inflammation. Treatment of SAD rats with sRAGE restored aortic NO formation through upregulating eNOS and dimethylarginine dimethylaminohydrolase-2 and downregulating protein arginine methyltransferase-1. Conclusion Activated RAGE contributed to aortic remodeling and endothelial dysfunction in SAD rats, possibly via induction of oxidative stress and inflammation, impairment of mitochondrial function, and reduction in NO bioavailability.</description><subject>advanced glycation end products</subject><subject>aldehyde reductase</subject><subject>Aldehyde Reductase - metabolism</subject><subject>Animals</subject><subject>Aorta - innervation</subject><subject>Aorta - metabolism</subject><subject>Aorta - physiopathology</subject><subject>Aortic remodeling</subject><subject>arginine</subject><subject>atherosclerosis</subject><subject>Autonomic Denervation</subject><subject>Baroreflex - physiology</subject><subject>bioavailability</subject><subject>Cardiovascular</subject><subject>Cardiovascular Diseases - metabolism</subject><subject>Cardiovascular Diseases - physiopathology</subject><subject>collagen</subject><subject>Disease Models, Animal</subject><subject>Endothelial dysfunction</subject><subject>endothelial nitric oxide synthase</subject><subject>Endothelium, Vascular - innervation</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Endothelium, Vascular - physiopathology</subject><subject>Inflammation</subject><subject>Lactoylglutathione Lyase - metabolism</subject><subject>Male</subject><subject>malondialdehyde</subject><subject>Mitochondria - metabolism</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - metabolism</subject><subject>Nitric Oxide Synthase Type III - metabolism</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - physiology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>reactive oxygen species</subject><subject>Receptor for Advanced Glycation End Products</subject><subject>Receptors, Immunologic - metabolism</subject><subject>Sinoaortic denervation</subject><subject>Vasculitis - metabolism</subject><subject>Vasculitis - physiopathology</subject><issn>0021-9150</issn><issn>1879-1484</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNks2O0zAUhSMEYsrAK4A3SGxSfOP8OAuQRiMYkEZiMYzEznLsm-KS2sV2KvVBeF9uaGExKxb-WZxz7vX9XBSvga-BQ_t2u9b5O8aQzLTsLq0rDmLN6zUX4lGxAtn1JdSyflysOK-g7KHhF8WzlLac87oD-bS4qISUHDq5Kn5dmewOOrvgWRhZRIP7HCIbaWl70N6gZZvpaE4S9JbtY7CzyYmZ4HN0w5wxsRyYDjE7QxG7YHFyfsM0qckRqOHJ6YnZYxpnb_4kOc-S8-FssugxUhtULOqcnhdPRj0lfHE-L4v7jx--Xn8qb7_cfL6-ui1NI_tcjiiGoYZWouBDJ2QrobJDJUYtAKDjemhbsL3VUugaW11B1fR2sI1uRjn0KC6LN6dcetPPGVNWO5cMTpP2GOakoCZHIxtoSPruJDU09RRxVPvodjoeFXC1kFFb9YCMWsgoXisiQ_6X51LzsEP7z_0XBQlenQSjDkpvIvnv7yihWbD10HWkuDkpkEZycBhVMg4XQo64ZWWD--9m3j9IMgTMGT39wCOmbZijp7krUKlSXN0tH2n5RyDo1jXfxG_GJcws</recordid><startdate>20130801</startdate><enddate>20130801</enddate><creator>Wu, Feng</creator><creator>Feng, Jin-Zhong</creator><creator>Qiu, Yi-Hua</creator><creator>Yu, Feng-Bin</creator><creator>Zhang, Jian-Zhong</creator><creator>Zhou, Wei</creator><creator>Yu, Feng</creator><creator>Wang, Guo-Kun</creator><creator>An, Li-Na</creator><creator>Ni, Fei-Hua</creator><creator>Wu, Hong</creator><creator>Zhao, Xian-Xian</creator><creator>Qin, Yong-Wen</creator><creator>Luo, He-De</creator><general>Elsevier Ireland Ltd</general><scope>FBQ</scope><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>7X8</scope></search><sort><creationdate>20130801</creationdate><title>Activation of receptor for advanced glycation end products contributes to aortic remodeling and endothelial dysfunction in sinoaortic denervated rats</title><author>Wu, Feng ; Feng, Jin-Zhong ; Qiu, Yi-Hua ; Yu, Feng-Bin ; Zhang, Jian-Zhong ; Zhou, Wei ; Yu, Feng ; Wang, Guo-Kun ; An, Li-Na ; Ni, Fei-Hua ; Wu, Hong ; Zhao, Xian-Xian ; Qin, Yong-Wen ; Luo, He-De</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c589t-fe3bb4168e30b7386812db23fa311170ab661d9da83a4e6a21259dbd5a5f8b9e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>advanced glycation end products</topic><topic>aldehyde reductase</topic><topic>Aldehyde Reductase - metabolism</topic><topic>Animals</topic><topic>Aorta - innervation</topic><topic>Aorta - metabolism</topic><topic>Aorta - physiopathology</topic><topic>Aortic remodeling</topic><topic>arginine</topic><topic>atherosclerosis</topic><topic>Autonomic Denervation</topic><topic>Baroreflex - physiology</topic><topic>bioavailability</topic><topic>Cardiovascular</topic><topic>Cardiovascular Diseases - metabolism</topic><topic>Cardiovascular Diseases - physiopathology</topic><topic>collagen</topic><topic>Disease Models, Animal</topic><topic>Endothelial dysfunction</topic><topic>endothelial nitric oxide synthase</topic><topic>Endothelium, Vascular - innervation</topic><topic>Endothelium, Vascular - metabolism</topic><topic>Endothelium, Vascular - physiopathology</topic><topic>Inflammation</topic><topic>Lactoylglutathione Lyase - metabolism</topic><topic>Male</topic><topic>malondialdehyde</topic><topic>Mitochondria - metabolism</topic><topic>Nitric oxide</topic><topic>Nitric Oxide - metabolism</topic><topic>Nitric Oxide Synthase Type III - metabolism</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - physiology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>reactive oxygen species</topic><topic>Receptor for Advanced Glycation End Products</topic><topic>Receptors, Immunologic - metabolism</topic><topic>Sinoaortic denervation</topic><topic>Vasculitis - metabolism</topic><topic>Vasculitis - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wu, Feng</creatorcontrib><creatorcontrib>Feng, Jin-Zhong</creatorcontrib><creatorcontrib>Qiu, Yi-Hua</creatorcontrib><creatorcontrib>Yu, Feng-Bin</creatorcontrib><creatorcontrib>Zhang, Jian-Zhong</creatorcontrib><creatorcontrib>Zhou, Wei</creatorcontrib><creatorcontrib>Yu, Feng</creatorcontrib><creatorcontrib>Wang, Guo-Kun</creatorcontrib><creatorcontrib>An, Li-Na</creatorcontrib><creatorcontrib>Ni, Fei-Hua</creatorcontrib><creatorcontrib>Wu, Hong</creatorcontrib><creatorcontrib>Zhao, Xian-Xian</creatorcontrib><creatorcontrib>Qin, Yong-Wen</creatorcontrib><creatorcontrib>Luo, He-De</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Atherosclerosis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wu, Feng</au><au>Feng, Jin-Zhong</au><au>Qiu, Yi-Hua</au><au>Yu, Feng-Bin</au><au>Zhang, Jian-Zhong</au><au>Zhou, Wei</au><au>Yu, Feng</au><au>Wang, Guo-Kun</au><au>An, Li-Na</au><au>Ni, Fei-Hua</au><au>Wu, Hong</au><au>Zhao, Xian-Xian</au><au>Qin, Yong-Wen</au><au>Luo, He-De</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Activation of receptor for advanced glycation end products contributes to aortic remodeling and endothelial dysfunction in sinoaortic denervated rats</atitle><jtitle>Atherosclerosis</jtitle><addtitle>Atherosclerosis</addtitle><date>2013-08-01</date><risdate>2013</risdate><volume>229</volume><issue>2</issue><spage>287</spage><epage>294</epage><pages>287-294</pages><issn>0021-9150</issn><eissn>1879-1484</eissn><abstract>Abstract Objective The aim of present study was to test the hypothesis that activation of receptor for advanced glycation end products (RAGE) pathway contributes to aortic remodeling and endothelial dysfunction in sinoaortic denervated (SAD) rats. Methods and results Experiment 1 : 8 weeks after sinoaortic denervation, aortas were removed for measurement of AGE/RAGE pathway. Sinoaortic denervation in rats resulted in enhanced activity of aldose reductase, reduced activity of glyoxalase 1, accumulation of methylglyoxal and AGE, and upregulated expression of RAGE in aortas. Experiment 2 : 5 weeks after sinoaortic denervation, the rats received intraperitoneal injections of 500 μg soluble RAGE (sRAGE) daily for 3 weeks. Treatment of SAD rats with sRAGE attenuated aortic remodeling, marked by reduction in AW/length, wall thickness, proliferation of SMC, and collagen deposition, and improvement of endothelial function. Treatment of SAD rats with sRAGE abated aortic oxidative stress, marked by reduction in formation of malondialdehyde, reactive oxygen species, superoxide, peroxynitrite and 3-nitrotyrosine, and enhancement of ratio of GSH/GSSG. Treatment of SAD rats with sRAGE attenuated aortic mitochondrial dysfunction. Treatment of SAD rats with sRAGE suppressed aortic NFκB nuclear translocation and inflammation. Treatment of SAD rats with sRAGE restored aortic NO formation through upregulating eNOS and dimethylarginine dimethylaminohydrolase-2 and downregulating protein arginine methyltransferase-1. Conclusion Activated RAGE contributed to aortic remodeling and endothelial dysfunction in SAD rats, possibly via induction of oxidative stress and inflammation, impairment of mitochondrial function, and reduction in NO bioavailability.</abstract><cop>Ireland</cop><pub>Elsevier Ireland Ltd</pub><pmid>23880178</pmid><doi>10.1016/j.atherosclerosis.2013.04.033</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | advanced glycation end products aldehyde reductase Aldehyde Reductase - metabolism Animals Aorta - innervation Aorta - metabolism Aorta - physiopathology Aortic remodeling arginine atherosclerosis Autonomic Denervation Baroreflex - physiology bioavailability Cardiovascular Cardiovascular Diseases - metabolism Cardiovascular Diseases - physiopathology collagen Disease Models, Animal Endothelial dysfunction endothelial nitric oxide synthase Endothelium, Vascular - innervation Endothelium, Vascular - metabolism Endothelium, Vascular - physiopathology Inflammation Lactoylglutathione Lyase - metabolism Male malondialdehyde Mitochondria - metabolism Nitric oxide Nitric Oxide - metabolism Nitric Oxide Synthase Type III - metabolism Oxidative stress Oxidative Stress - physiology Rats Rats, Sprague-Dawley reactive oxygen species Receptor for Advanced Glycation End Products Receptors, Immunologic - metabolism Sinoaortic denervation Vasculitis - metabolism Vasculitis - physiopathology |
| title | Activation of receptor for advanced glycation end products contributes to aortic remodeling and endothelial dysfunction in sinoaortic denervated rats |
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