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These compounds accumulate in a number of chronic disease states, contributing to tissue injury via several mechanisms, including activation of the receptor for advanced glycation end products (<jats:styled-content style=\"fixed-case\">RAGE<\/jats:styled-content>). We aimed to investigate whether <jats:styled-content style=\"fixed-case\">AGE<\/jats:styled-content>s can exacerbate chronic liver injury and contribute to hepatic fibrosis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We initially studied the effects of chronic hepatic exposure to high levels of <jats:styled-content style=\"fixed-case\">AGE<\/jats:styled-content>s given intraperitoneally as <jats:styled-content style=\"fixed-case\">AGE<\/jats:styled-content>\u2010rat serum albumin. In a separate experiment, we examined the impact of high <jats:styled-content style=\"fixed-case\">AGE<\/jats:styled-content> exposure in rats following bile duct ligation (<jats:styled-content style=\"fixed-case\">BDL<\/jats:styled-content>).<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>In normal rats, chronic <jats:styled-content style=\"fixed-case\">AGE<\/jats:styled-content>\u2010rat serum albumin administration induced significant increases in \u03b1\u2010smooth muscle actin gene and protein expression but did not induce fibrosis or biochemical evidence of liver injury. However, in <jats:styled-content style=\"fixed-case\">BDL<\/jats:styled-content> animals, <jats:styled-content style=\"fixed-case\">AGE<\/jats:styled-content>\u2010bovine serum albumin administration significantly increased hepatic fibrosis as evidenced by increased collagen content and \u03b1\u2010smooth muscle actin expression, compared with <jats:styled-content style=\"fixed-case\">BDL<\/jats:styled-content> alone. Furthermore, <jats:styled-content style=\"fixed-case\">AGE<\/jats:styled-content>s increased hepatic oxidative stress and receptor for advanced glycation end products gene expression.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>These findings suggest that <jats:styled-content style=\"fixed-case\">AGE<\/jats:styled-content>s may contribute to the pathogenesis of chronic liver injury and fibrosis.<\/jats:p><\/jats:sec>","DOI":"10.1111\/jgh.12042","type":"journal-article","created":{"date-parts":[[2012,11,22]],"date-time":"2012-11-22T18:43:24Z","timestamp":1353609804000},"page":"369-376","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":56,"title":["Advanced glycation end products augment experimental hepatic fibrosis"],"prefix":"10.1111","volume":"28","author":[{"given":"Michelle","family":"Goodwin","sequence":"first","affiliation":[{"name":"Department of Medicine The University of Melbourne  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