University of Oulu

Richter, K. & Kietzmann, T. Cell Tissue Res (2016) 365: 591. doi:10.1007/s00441-016-2445-3

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

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Author: Richter, Kati1; Kietzmann, Thomas1
Organizations: 1Faculty of Biochemistry and Molecular Medicine and Biocenter Oulu, University of Oulu, Oulu, Finland
Format: article
Version: published version
Access: open
Online Access: PDF Full Text (PDF, 1.3 MB)
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Language: English
Published: Springer Nature, 2016
Publish Date: 2017-02-27


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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Series: Cell and tissue research
ISSN: 0302-766X
ISSN-E: 1432-0878
ISSN-L: 0302-766X
Volume: 365
Issue: 3
Pages: 591 - 605
DOI: 10.1007/s00441-016-2445-3
Type of Publication: A1 Journal article – refereed
Field of Science: 3111 Biomedicine
Copyright information: © The Author(s) 2016. This article is published with open access at This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (, 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.