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Mitochondrial reactive oxygen species drive proinflammatory cytokine production

High levels of reactive oxygen species (ROS) are observed in chronic human diseases such as neurodegeneration, Crohn’s disease, and cancer. In addition to the presence of oxidative stress, these diseases are also characterized by deregulated inflammatory responses, including but not limited to proin...

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Detalles Bibliográficos
Autores principales: Naik, Edwina, Dixit, Vishva M.
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3058577/
https://www.ncbi.nlm.nih.gov/pubmed/21357740
http://dx.doi.org/10.1084/jem.20110367
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author Naik, Edwina
Dixit, Vishva M.
author_facet Naik, Edwina
Dixit, Vishva M.
author_sort Naik, Edwina
collection PubMed
description High levels of reactive oxygen species (ROS) are observed in chronic human diseases such as neurodegeneration, Crohn’s disease, and cancer. In addition to the presence of oxidative stress, these diseases are also characterized by deregulated inflammatory responses, including but not limited to proinflammatory cytokine production. New work exploring the mechanisms linking ROS and inflammation find that ROS derived from mitochondria act as signal-transducing molecules that provoke the up-regulation of inflammatory cytokine subsets via distinct molecular pathways.
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spelling pubmed-30585772011-09-14 Mitochondrial reactive oxygen species drive proinflammatory cytokine production Naik, Edwina Dixit, Vishva M. J Exp Med Minireview High levels of reactive oxygen species (ROS) are observed in chronic human diseases such as neurodegeneration, Crohn’s disease, and cancer. In addition to the presence of oxidative stress, these diseases are also characterized by deregulated inflammatory responses, including but not limited to proinflammatory cytokine production. New work exploring the mechanisms linking ROS and inflammation find that ROS derived from mitochondria act as signal-transducing molecules that provoke the up-regulation of inflammatory cytokine subsets via distinct molecular pathways. The Rockefeller University Press 2011-03-14 /pmc/articles/PMC3058577/ /pubmed/21357740 http://dx.doi.org/10.1084/jem.20110367 Text en © 2011 Naik and Dixit This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).
spellingShingle Minireview
Naik, Edwina
Dixit, Vishva M.
Mitochondrial reactive oxygen species drive proinflammatory cytokine production
title Mitochondrial reactive oxygen species drive proinflammatory cytokine production
title_full Mitochondrial reactive oxygen species drive proinflammatory cytokine production
title_fullStr Mitochondrial reactive oxygen species drive proinflammatory cytokine production
title_full_unstemmed Mitochondrial reactive oxygen species drive proinflammatory cytokine production
title_short Mitochondrial reactive oxygen species drive proinflammatory cytokine production
title_sort mitochondrial reactive oxygen species drive proinflammatory cytokine production
topic Minireview
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3058577/
https://www.ncbi.nlm.nih.gov/pubmed/21357740
http://dx.doi.org/10.1084/jem.20110367
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