Reactive oxygen species and fibrosis : further evidence of a significant liaison
Richter, Kati; Kietzmann, Thomas (2016-06-27)
Richter, K. & Kietzmann, T. Cell Tissue Res (2016) 365: 591. doi:10.1007/s00441-016-2445-3
© The Author(s) 2016. This article is published with open access at Springerlink.com 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.
https://creativecommons.org/licenses/by/4.0/
https://urn.fi/URN:NBN:fi-fe201702271880
Tiivistelmä
Abstract
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.
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