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dc.contributor.authorMandrekar, Pranoti
dc.date2022-08-11T08:09:33.000
dc.date.accessioned2022-08-23T16:35:09Z
dc.date.available2022-08-23T16:35:09Z
dc.date.issued2007-09-15
dc.date.submitted2009-03-16
dc.identifier.citationWorld J Gastroenterol. 2007 Oct 7;13(37):4979-85. <a href="http://www.wjgnet.com/1007-9327/13/4979.asp">Link to article on publisher's website</a>
dc.identifier.issn1007-9327 (Print)
dc.identifier.pmid17854141
dc.identifier.urihttp://hdl.handle.net/20.500.14038/38495
dc.description.abstractAlcoholic liver injury comprises of interactions of various intracellular signaling events in the liver. Innate immune responses in the resident Kupffer cells of the liver, oxidative stress-induced activation of hepatocytes, fibrotic events in liver stellate cells and activation of liver sinusoidal endothelial cells all contribute to alcoholic liver injury. The signaling mechanisms associated with alcoholic liver injury vary based on the cell type involved and the extent of alcohol consumption. In this review we will elucidate the oxidative stress and signaling pathways affected by alcohol in hepatocytes and Kupffer cells in the liver by alcohol. The toll-like receptors and their down-stream signaling events that play an important role in alcohol-induced inflammation will be discussed. Alcohol-induced alterations of various intracellular transcription factors such as NFkappaB, PPARs and AP-1, as well as MAPK kinases in hepatocytes and macrophages leading to induction of target genes that contribute to liver injury will be reviewed. Finally, we will discuss the significance of heat shock proteins as chaperones and their functional regulation in the liver that could provide new mechanistic insights into the contributions of stress-induced signaling mechanisms in alcoholic liver injury.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=17854141&dopt=Abstract">Link to Article in PubMed</a>
dc.subjectHeat-Shock Proteins
dc.subjectHumans
dc.subjectLiver Diseases, Alcoholic
dc.subjectMitogen-Activated Protein Kinase Kinases
dc.subjectOxidative Stress
dc.subjectSignal Transduction
dc.subjectToll-Like Receptors
dc.subjectTranscription Factors
dc.subjectGastroenterology
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleSignaling mechanisms in alcoholic liver injury: role of transcription factors, kinases and heat shock proteins
dc.typeJournal Article
dc.source.journaltitleWorld journal of gastroenterology : WJG
dc.source.volume13
dc.source.issue37
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=2367&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/1368
dc.identifier.contextkey783052
refterms.dateFOA2022-08-23T16:35:10Z
html.description.abstract<p>Alcoholic liver injury comprises of interactions of various intracellular signaling events in the liver. Innate immune responses in the resident Kupffer cells of the liver, oxidative stress-induced activation of hepatocytes, fibrotic events in liver stellate cells and activation of liver sinusoidal endothelial cells all contribute to alcoholic liver injury. The signaling mechanisms associated with alcoholic liver injury vary based on the cell type involved and the extent of alcohol consumption. In this review we will elucidate the oxidative stress and signaling pathways affected by alcohol in hepatocytes and Kupffer cells in the liver by alcohol. The toll-like receptors and their down-stream signaling events that play an important role in alcohol-induced inflammation will be discussed. Alcohol-induced alterations of various intracellular transcription factors such as NFkappaB, PPARs and AP-1, as well as MAPK kinases in hepatocytes and macrophages leading to induction of target genes that contribute to liver injury will be reviewed. Finally, we will discuss the significance of heat shock proteins as chaperones and their functional regulation in the liver that could provide new mechanistic insights into the contributions of stress-induced signaling mechanisms in alcoholic liver injury.</p>
dc.identifier.submissionpathoapubs/1368
dc.contributor.departmentDepartment of Medicine, Rheumatology Division
dc.contributor.departmentLiver Center
dc.source.pages4979-85


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