Richter Kati, Kietzmann Thomas
Faculty of Biochemistry and Molecular Medicine and Biocenter Oulu, University of Oulu, Aapistie 7A, FI-90230, Oulu, Finland.
Cell Tissue Res. 2016 Sep;365(3):591-605. doi: 10.1007/s00441-016-2445-3. Epub 2016 Jun 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. Graphical abstract ᅟ.
肥胖、糖尿病、非酒精性脂肪性肝病、慢性肾脏病和心肌病等与年龄相关的疾病常伴有纤维化。过去十年的研究增进了我们对促成纤维化发展的病理生理机制的理解。特别是，氧化应激和抗氧化系统似乎是转化生长因子-β1（TGF-β1）信号传导、代谢稳态和慢性低度炎症等过程的关键调节因子，所有这些过程在纤维化的发展和持续中都起着重要作用。在本综述中，我们讨论了活性氧、抗氧化酶与TGF-β1信号传导之间的联系以及功能后果，反映了一种氧化还原纤维化的概念，可作为未来治疗的靶点。图形摘要ᅟ。
