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

被引:226
作者
Richter, Kati [1 ,2 ]
Kietzmann, Thomas [1 ,2 ]
机构
[1] Univ Oulu, Fac Biochem & Mol Med, Aapistie 7A, FI-90230 Oulu, Finland
[2] Univ Oulu, Bioctr Oulu, Aapistie 7A, FI-90230 Oulu, Finland
基金
芬兰科学院;
关键词
Reactive oxygen species (ROS); Antioxidants; Antioxidative enzymes; Matrix; Fibrosis; GROWTH-FACTOR-BETA; ADENINE-DINUCLEOTIDE PHOSPHATE; TO-MESENCHYMAL TRANSITION; STELLATE CELL ACTIVATION; CHRONIC HEPATITIS-C; OXIDATIVE STRESS; NADPH OXIDASE; TGF-BETA; PULMONARY-FIBROSIS; DNA METHYLATION;
D O I
10.1007/s00441-016-2445-3
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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-beta 1 (TGF-beta 1) 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-beta 1 signalling, together with functional consequences, reflecting a concept of redox-fibrosis that can be targeted in future therapies.
引用
收藏
页码:591 / 605
页数:15
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