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. Graphical abstract ᅟ.