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Reactive oxygen species and fibrosis: further evidence of a significant liaison

Age-related diseases such as obesity, diabetes, non-alcoholic fatty liver disease, chronic kidney disease and cardiomyopathy are frequently associated with fibrosis. Work within the last decade has improved our understanding of the pathophysiological mechanisms contributing to fibrosis development....

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Detalles Bibliográficos
Autores principales: Richter, Kati, Kietzmann, Thomas
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Berlin Heidelberg 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5010605/
https://www.ncbi.nlm.nih.gov/pubmed/27345301
http://dx.doi.org/10.1007/s00441-016-2445-3
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author Richter, Kati
Kietzmann, Thomas
author_facet Richter, Kati
Kietzmann, Thomas
author_sort Richter, Kati
collection PubMed
description Age-related diseases such as obesity, diabetes, non-alcoholic fatty liver disease, chronic kidney disease and cardiomyopathy are frequently associated with fibrosis. Work within the last decade has improved our understanding of the pathophysiological mechanisms contributing to fibrosis development. In particular, oxidative stress and the antioxidant system appear to be crucial modulators of processes such as transforming growth factor-β1 (TGF-β1) signalling, metabolic homeostasis and chronic low-grade inflammation, all of which play important roles in fibrosis development and persistence. In the current review, we discuss the connections between reactive oxygen species, antioxidant enzymes and TGF-β1 signalling, together with functional consequences, reflecting a concept of redox-fibrosis that can be targeted in future therapies. [Figure: see text]
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spelling pubmed-50106052016-09-16 Reactive oxygen species and fibrosis: further evidence of a significant liaison Richter, Kati Kietzmann, Thomas Cell Tissue Res Review Age-related diseases such as obesity, diabetes, non-alcoholic fatty liver disease, chronic kidney disease and cardiomyopathy are frequently associated with fibrosis. Work within the last decade has improved our understanding of the pathophysiological mechanisms contributing to fibrosis development. In particular, oxidative stress and the antioxidant system appear to be crucial modulators of processes such as transforming growth factor-β1 (TGF-β1) signalling, metabolic homeostasis and chronic low-grade inflammation, all of which play important roles in fibrosis development and persistence. In the current review, we discuss the connections between reactive oxygen species, antioxidant enzymes and TGF-β1 signalling, together with functional consequences, reflecting a concept of redox-fibrosis that can be targeted in future therapies. [Figure: see text] Springer Berlin Heidelberg 2016-06-27 2016 /pmc/articles/PMC5010605/ /pubmed/27345301 http://dx.doi.org/10.1007/s00441-016-2445-3 Text en © The Author(s) 2016 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
spellingShingle Review
Richter, Kati
Kietzmann, Thomas
Reactive oxygen species and fibrosis: further evidence of a significant liaison
title Reactive oxygen species and fibrosis: further evidence of a significant liaison
title_full Reactive oxygen species and fibrosis: further evidence of a significant liaison
title_fullStr Reactive oxygen species and fibrosis: further evidence of a significant liaison
title_full_unstemmed Reactive oxygen species and fibrosis: further evidence of a significant liaison
title_short Reactive oxygen species and fibrosis: further evidence of a significant liaison
title_sort reactive oxygen species and fibrosis: further evidence of a significant liaison
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5010605/
https://www.ncbi.nlm.nih.gov/pubmed/27345301
http://dx.doi.org/10.1007/s00441-016-2445-3
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