{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,6,11]],"date-time":"2025-06-11T04:24:23Z","timestamp":1749615863769},"reference-count":49,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2013,6,13]],"date-time":"2013-06-13T00:00:00Z","timestamp":1371081600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Alcoholism Clin &amp; Exp Res"],"published-print":{"date-parts":[[2013,10]]},"abstract":"Background<\/jats:title>Because the histological and biochemical progression of liver disease is similar in alcoholic steatohepatitis (ASH<\/jats:styled-content>) and nonalcoholic steatohepatitis (NASH<\/jats:styled-content>), we hypothesized that the genetic susceptibility to these liver diseases would be similar. To identify potential candidate genes that regulate the development of liver fibrosis, we studied a chromosome substitution strain (CSS<\/jats:styled-content>\u201017) that contains chromosome 17 from the A<\/jats:styled-content>\/J<\/jats:styled-content> inbred strain substituted for the corresponding chromosome on the C<\/jats:styled-content>57BL<\/jats:styled-content>\/6J<\/jats:styled-content> (B6) genetic background. Previously, we identified quantitative trait loci (QTL<\/jats:styled-content>s) in CSS<\/jats:styled-content>\u201017, namely obesity\u2010resistant QTL<\/jats:styled-content> 13 and QTL<\/jats:styled-content> 15 (Obrq13<\/jats:italic><\/jats:styled-content> and Obrq15<\/jats:italic><\/jats:styled-content>, respectively), that were associated with protection from diet\u2010induced obesity and hepatic steatosis on a high\u2010fat diet.<\/jats:p><\/jats:sec>Methods<\/jats:title>To test whether these or other CSS<\/jats:styled-content>\u201017 QTL<\/jats:styled-content>s conferred resistance to alcohol\u2010induced liver injury and fibrosis, B<\/jats:styled-content>6, A<\/jats:styled-content>\/J<\/jats:styled-content>, CSS<\/jats:styled-content>\u201017, and congenics 17C<\/jats:styled-content>\u20101 and 17C<\/jats:styled-content>\u20106 were either fed L<\/jats:styled-content>ieber\u2013D<\/jats:styled-content>eC<\/jats:styled-content>arli ethanol (E<\/jats:styled-content>tOH<\/jats:styled-content>)\u2010containing diet or had carbon tetrachloride (CC<\/jats:styled-content>l4<\/jats:sub>) administered chronically.<\/jats:p><\/jats:sec>Results<\/jats:title>The congenic strain carrying Obrq15<\/jats:italic><\/jats:styled-content> showed resistance from alcohol\u2010induced liver injury and liver fibrosis, whereas Obrq13<\/jats:italic><\/jats:styled-content> conferred susceptibility to liver fibrosis. From published deep sequencing data for chromosome 17 in the B<\/jats:styled-content>6 and A<\/jats:styled-content>\/J<\/jats:styled-content> strains, we identified candidate genes in Obrq13<\/jats:italic><\/jats:styled-content> and Obrq15<\/jats:italic><\/jats:styled-content> that contained single\u2010nucleotide polymorphisms (SNP<\/jats:styled-content>s) in the promoter region or within the gene itself. NADPH<\/jats:styled-content> oxidase organizer 1 (Noxo1<\/jats:italic><\/jats:styled-content>) and NLR<\/jats:styled-content> family, CARD<\/jats:styled-content> domain containing 4 (Nlrc4<\/jats:italic><\/jats:styled-content>) showed altered hepatic gene expression in strains with the A<\/jats:styled-content>\/J<\/jats:styled-content> allele at the end of the E<\/jats:styled-content>tOH<\/jats:styled-content> diet study and after CC<\/jats:styled-content>l4<\/jats:sub> treatment.<\/jats:p><\/jats:sec>Conclusions<\/jats:title>Aspects of the genetics for the progression of ASH<\/jats:styled-content> are unique compared to NASH<\/jats:styled-content>, suggesting that the molecular mechanisms for the progression of disease are at least partially distinct. Using these CSS<\/jats:styled-content>s, we identified 2 candidate genes, Noxo1<\/jats:italic><\/jats:styled-content> and Nlrc4<\/jats:italic><\/jats:styled-content>, which modulate genetic susceptibility in ASH<\/jats:styled-content>.<\/jats:p><\/jats:sec>","DOI":"10.1111\/acer.12157","type":"journal-article","created":{"date-parts":[[2013,6,13]],"date-time":"2013-06-13T15:20:05Z","timestamp":1371136805000},"page":"1668-1679","source":"Crossref","is-referenced-by-count":9,"title":["Genetic Resistance to Liver Fibrosis on A\/J Mouse Chromosome 17"],"prefix":"10.1111","volume":"37","author":[{"given":"David A.","family":"DeSantis","sequence":"first","affiliation":[{"name":"Department of Nutrition Case Western Reserve University School of Medicine Cleveland Ohio"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Peter","family":"Lee","sequence":"additional","affiliation":[{"name":"Department of Nutrition Case Western Reserve University School of Medicine Cleveland 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