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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.

Item Type:	Refereed Article
Keywords:	fibrosis, NADPH oxidase, Nox4, Redox signaling, transforming growth factor-β
Research Division:	Biomedical and Clinical Sciences
Research Group:	Medical biotechnology
Research Field:	Gene and molecular therapy
Objective Division:	Health
Objective Group:	Clinical health
Objective Field:	Clinical health not elsewhere classified
UTAS Author:	Liu, GS (Associate Professor Guei-Sheung Liu)
ID Code:	120862
Year Published:	2014
Web of Science® Times Cited:	178
Deposited By:	Menzies Institute for Medical Research
Deposited On:	2017-08-31
Last Modified:	2017-11-03
Downloads:	119 View Download Statistics