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Oxidative Stress and Inflammation: Essential Partners in Alcoholic Liver Disease

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 sensitizat...

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Detalles Bibliográficos
Autores principales: Ambade, Aditya, Mandrekar, Pranoti
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3303590/
https://www.ncbi.nlm.nih.gov/pubmed/22500241
http://dx.doi.org/10.1155/2012/853175
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author Ambade, Aditya
Mandrekar, Pranoti
author_facet Ambade, Aditya
Mandrekar, Pranoti
author_sort Ambade, Aditya
collection PubMed
description 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.
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spelling pubmed-33035902012-04-12 Oxidative Stress and Inflammation: Essential Partners in Alcoholic Liver Disease Ambade, Aditya Mandrekar, Pranoti Int J Hepatol Review Article 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. Hindawi Publishing Corporation 2012 2012-03-01 /pmc/articles/PMC3303590/ /pubmed/22500241 http://dx.doi.org/10.1155/2012/853175 Text en Copyright © 2012 A. Ambade and P. Mandrekar. https://creativecommons.org/licenses/by/3.0/ 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.
spellingShingle Review Article
Ambade, Aditya
Mandrekar, Pranoti
Oxidative Stress and Inflammation: Essential Partners in Alcoholic Liver Disease
title Oxidative Stress and Inflammation: Essential Partners in Alcoholic Liver Disease
title_full Oxidative Stress and Inflammation: Essential Partners in Alcoholic Liver Disease
title_fullStr Oxidative Stress and Inflammation: Essential Partners in Alcoholic Liver Disease
title_full_unstemmed Oxidative Stress and Inflammation: Essential Partners in Alcoholic Liver Disease
title_short Oxidative Stress and Inflammation: Essential Partners in Alcoholic Liver Disease
title_sort oxidative stress and inflammation: essential partners in alcoholic liver disease
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3303590/
https://www.ncbi.nlm.nih.gov/pubmed/22500241
http://dx.doi.org/10.1155/2012/853175
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