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Redox Biol. 2014 Jan 20;2:267-72. doi: 10.1016/j.redox.2014.01.012. eCollection 2014.

NADPH oxidase-dependent redox signaling in TGF-β-mediated fibrotic responses.

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Key Laboratory of Cardiovascular Remodeling and Function Research, Qilu Hospital, Shandong University, Jinan, Shandong 250012, China.
Centre for Eye Research Australia, University of Melbourne, VIC 3002, Australia ; Department of Ophthalmology, University of Melbourne, VIC 3002, Australia.
Centre for Eye Research Australia, University of Melbourne, VIC 3002, Australia.


Uncontrolled fibrosis in organs like heart, kidney, liver and lung is detrimental and may lead to end-stage organ failure. Currently there is no effective treatment for fibrotic disorders. Transforming growth factor (TGF)-β has a fundamental role in orchestrating the process of fibrogenesis; however, interventions directly targeting TGF-β would have undesired systemic side effects due to the multiple physiological functions of TGF-β. Further characterization of the downstream signaling pathway(s) involved in TGF-β-mediated fibrosis may lead to discovery of novel treatment strategies for fibrotic disorders. Accumulating evidence suggests that Nox4 NADPH oxidase may be an important downstream effector in mediating TGF-β-induced fibrosis, while NADPH oxidase-dependent redox signaling may in turn regulate TGF-β/Smad signaling in a feed-forward manner. It is proposed that pharmacological inhibition of the Nox4 function may represent a novel approach in treatment of fibrotic disorders.


Fibrosis; NADPH oxidase; Nox4; Redox signaling; Transforming growth factor-β

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