Oxidative stress and inflammation: essential partners in alcoholic liver disease
| dc.contributor.author | Ambade, Aditya | |
| dc.contributor.author | Mandrekar, Pranoti | |
| dc.date | 2022-08-11T08:11:05.000 | |
| dc.date.accessioned | 2022-08-23T17:32:38Z | |
| dc.date.available | 2022-08-23T17:32:38Z | |
| dc.date.issued | 2012-03-01 | |
| dc.date.submitted | 2012-06-22 | |
| 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.issn | 2090-3456 (Electronic) | |
| dc.identifier.doi | 10.1155/2012/853175 | |
| dc.identifier.pmid | 22500241 | |
| dc.identifier.uri | http://hdl.handle.net/20.500.14038/50992 | |
| dc.description.abstract | 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. | |
| dc.language.iso | en_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.url | http://dx.doi.org/10.1155/2012/853175 | |
| dc.rights | 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. | |
| dc.rights.uri | http://creativecommons.org/licenses/by/3.0/ | |
| dc.subject | Liver Diseases, Alcoholic | |
| dc.subject | Oxidative Stress | |
| dc.subject | Inflammation | |
| dc.subject | Digestive System Diseases | |
| dc.subject | Gastroenterology | |
| dc.subject | Hepatology | |
| dc.title | Oxidative stress and inflammation: essential partners in alcoholic liver disease | |
| dc.type | Journal Article | |
| dc.source.journaltitle | International journal of hepatology | |
| dc.source.volume | 2012 | |
| dc.identifier.legacyfulltext | https://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=1526&context=wfc_pp&unstamped=1 | |
| dc.identifier.legacycoverpage | https://escholarship.umassmed.edu/wfc_pp/527 | |
| dc.identifier.contextkey | 3017584 | |
| refterms.dateFOA | 2022-08-23T17:32:38Z | |
| 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.submissionpath | wfc_pp/527 | |
| dc.contributor.department | Department of Medicine, Division of Gastroenterology | |
| dc.source.pages | 853175 |

