Show simple item record

dc.contributor.authorSzabo, Gyongyi
dc.contributor.authorIracheta-Vellve, Arvin
dc.date2022-08-11T08:08:34.000
dc.date.accessioned2022-08-23T15:59:24Z
dc.date.available2022-08-23T15:59:24Z
dc.date.issued2015-09-01
dc.date.submitted2016-05-09
dc.identifier.citationClin Res Hepatol Gastroenterol. 2015 Sep;39 Suppl 1:S18-23. doi: 10.1016/j.clinre.2015.06.012. Epub 2015 Jul 26. <a href="http://dx.doi.org/10.1016/j.clinre.2015.06.012">Link to article on publisher's site</a>
dc.identifier.issn2210-7401 (Linking)
dc.identifier.doi10.1016/j.clinre.2015.06.012
dc.identifier.pmid26216030
dc.identifier.urihttp://hdl.handle.net/20.500.14038/30660
dc.description<p>Co-author Arvin Iracheta-Vellve is a doctoral student in the Translational Science Program in the Graduate School of Biomedical Sciences (GSBS) at UMass Medical School.</p>
dc.description.abstractUpregulation of the inflammatory cascade is a major element both in the progression of steatohepatitis to severe alcoholic hepatitis as well as in the progression of NASH to advanced NASH with fibrosis. The mechanisms underpinning these changes are only partially understood. Activation of the inflammatory cascade requires multiple stimuli and in this report, we discuss the role of inflammasomes that activate IL-1beta as well as the sterile and pathogen-derived danger signals that results in inflammasome activation and inflammation in alcoholic and non-alcoholic steatohepatitis. The dynamics of inflammasome activation, the cell types involved and the trigger signals appear to be somewhat different between ASH and NASH. Further studies are needed to dissect the pathology-related differences between these two major forms of steatohepatitis. Clinical and therapeutic implications of inflammasome activation in steatohepatitis are also discussed.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=26216030&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1016/j.clinre.2015.06.012
dc.subjectDigestive System Diseases
dc.subjectGastroenterology
dc.subjectHepatology
dc.subjectImmunity
dc.subjectImmunopathology
dc.titleInflammasome activation in the liver: Focus on alcoholic and non-alcoholic steatohepatitis
dc.typeJournal Article
dc.source.journaltitleClinics and research in hepatology and gastroenterology
dc.source.volume39 Suppl 1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/faculty_pubs/937
dc.identifier.contextkey8575149
html.description.abstract<p>Upregulation of the inflammatory cascade is a major element both in the progression of steatohepatitis to severe alcoholic hepatitis as well as in the progression of NASH to advanced NASH with fibrosis. The mechanisms underpinning these changes are only partially understood. Activation of the inflammatory cascade requires multiple stimuli and in this report, we discuss the role of inflammasomes that activate IL-1beta as well as the sterile and pathogen-derived danger signals that results in inflammasome activation and inflammation in alcoholic and non-alcoholic steatohepatitis. The dynamics of inflammasome activation, the cell types involved and the trigger signals appear to be somewhat different between ASH and NASH. Further studies are needed to dissect the pathology-related differences between these two major forms of steatohepatitis. Clinical and therapeutic implications of inflammasome activation in steatohepatitis are also discussed.</p>
dc.identifier.submissionpathfaculty_pubs/937
dc.contributor.departmentGraduate School of Biomedical Sciences
dc.contributor.departmentDepartment of Medicine, Division of Gastroenterology
dc.source.pagesS18-23


Files in this item

Thumbnail
Name:
Publisher version

This item appears in the following Collection(s)

Show simple item record