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dc.contributor.authorAmbade, Aditya
dc.contributor.authorMandrekar, Pranoti
dc.date2022-08-11T08:11:05.000
dc.date.accessioned2022-08-23T17:32:38Z
dc.date.available2022-08-23T17:32:38Z
dc.date.issued2012-03-01
dc.date.submitted2012-06-22
dc.identifier.citation<p>Int J Hepatol. 2012;2012:853175. <a href="http://dx.doi.org/10.1155/2012/853175" target="_blank">Link to article on publisher's site</a></p>
dc.identifier.issn2090-3456 (Electronic)
dc.identifier.doi10.1155/2012/853175
dc.identifier.pmid22500241
dc.identifier.urihttp://hdl.handle.net/20.500.14038/50992
dc.description.abstractAlcoholic liver disease (ALD) is a multifaceted disease that is characterized by hepatic steatosis or fat deposition and hepatitis or inflammation. Over the past decade, multiple lines of evidence have emerged on the mechanisms associated with ALD. The key mechanisms identified so far are sensitization to gut-derived endotoxin/lipopolysaccharide resulting in proinflammatory cytokine production and cellular stress due to oxidative processes, contributing to the development and progression of disease. While oxidative stress and inflammatory responses are studied independently in ALD, mechanisms linking these two processes play a major role in pathogenesis of disease. Here we review major players of oxidative stress and inflammation and highlight signaling intermediates regulated by oxidative stress that provokes proinflammatory responses in alcoholic liver disease.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=22500241&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttp://dx.doi.org/10.1155/2012/853175
dc.rightsCopyright © 2012 Aditya Ambade and Pranoti Mandrekar. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/
dc.subjectLiver Diseases, Alcoholic
dc.subjectOxidative Stress
dc.subjectInflammation
dc.subjectDigestive System Diseases
dc.subjectGastroenterology
dc.subjectHepatology
dc.titleOxidative stress and inflammation: essential partners in alcoholic liver disease
dc.typeJournal Article
dc.source.journaltitleInternational journal of hepatology
dc.source.volume2012
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=1526&amp;context=wfc_pp&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/wfc_pp/527
dc.identifier.contextkey3017584
refterms.dateFOA2022-08-23T17:32:38Z
html.description.abstract<p>Alcoholic liver disease (ALD) is a multifaceted disease that is characterized by hepatic steatosis or fat deposition and hepatitis or inflammation. Over the past decade, multiple lines of evidence have emerged on the mechanisms associated with ALD. The key mechanisms identified so far are sensitization to gut-derived endotoxin/lipopolysaccharide resulting in proinflammatory cytokine production and cellular stress due to oxidative processes, contributing to the development and progression of disease. While oxidative stress and inflammatory responses are studied independently in ALD, mechanisms linking these two processes play a major role in pathogenesis of disease. Here we review major players of oxidative stress and inflammation and highlight signaling intermediates regulated by oxidative stress that provokes proinflammatory responses in alcoholic liver disease.</p>
dc.identifier.submissionpathwfc_pp/527
dc.contributor.departmentDepartment of Medicine, Division of Gastroenterology
dc.source.pages853175


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Copyright © 2012 Aditya Ambade and Pranoti Mandrekar. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Except where otherwise noted, this item's license is described as Copyright © 2012 Aditya Ambade and Pranoti Mandrekar. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.