Format

Send to

Choose Destination
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.

Author information

1
Key Laboratory of Cardiovascular Remodeling and Function Research, Qilu Hospital, Shandong University, Jinan, Shandong 250012, China.
2
Centre for Eye Research Australia, University of Melbourne, VIC 3002, Australia ; Department of Ophthalmology, University of Melbourne, VIC 3002, Australia.
3
Centre for Eye Research Australia, University of Melbourne, VIC 3002, Australia.

Abstract

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.

KEYWORDS:

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

PMID:
24494202
PMCID:
PMC3909817
DOI:
10.1016/j.redox.2014.01.012
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Elsevier Science Icon for PubMed Central
Loading ...
Support Center