Signalling pathways from NADPH oxidase-4 to idiopathic pulmonary fibrosis

被引：56

作者：

Crestani, Bruno ^{[1
,2
,3
]}

Besnard, Valerie ^{[1
,2
]}

Boczkowski, Jorge ^{[4
,5
,6
,7
]}

机构：

[1] INSERM, U700, Paris, France

[2] Univ Paris 07, Paris, France

[3] Hop Bichat Claude Bernard, AP HP, Serv Pneumol A, Ctr Competence Malad Pulm Rares, F-75877 Paris, France

[4] Hop Henri Mondor, INSERM, U955, F-94010 Creteil, France

[5] Univ Paris Est Creteil, Fac Med, F-94010 Creteil, France

[6] Hop Henri Mondor, AP HP, Serv Explorat Fonct, F-94010 Creteil, France

[7] Hosp Intercommunal Creteil, Serv Pneumol & Pathol Profess, F-94000 Creteil, France

来源：

INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY | 2011年 / 43卷 / 08期

关键词：

NADPH oxidase; TGF-beta; Smad; Lung; Fibrosis; SMOOTH-MUSCLE-CELLS; ENDOPLASMIC-RETICULUM STRESS; REACTIVE OXYGEN; NOX4; DIFFERENTIATION; MYOFIBROBLASTS; ACTIVATION; APOPTOSIS; AIRWAY; PHOSPHORYLATION;

D O I：

10.1016/j.biocel.2011.04.003

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

This review focuses on the roles of NADPH oxidase/NOX proteins in idiopathic pulmonary fibrosis (IPF) pathophysiology and in the signalling pathways involved in IPF. NOX proteins are membrane-associated multi-unit enzymes that catalyze the reduction of oxygen using NADPH as an electron donor. Recent studies indicate that NOX4 is induced in pulmonary fibroblasts in response to TGF-beta. TGF-beta or PDGF induce myofibroblast proliferation, differentiation, migration, contractility and extracellular matrix production, through NOX4 and reactive oxygen species dependent SMAD2/3 phosphorylation. NOX4 is increased in pulmonary fibroblasts from IPF patients and deletion of Nox4 in mice prevents bleomycin-induced pulmonary fibrosis. These data strongly suggest that targeting of NOX4 could be a step forward in the treatment of fibrotic lung diseases, by specifically targeting myofibroblasts, a major player in this disease. (C) 2011 Elsevier Ltd. All rights reserved.

引用

页码：1086 / 1089

页数：4

共 30 条

[1] Diesel exhaust particles induce matrix metalloprotease-1 in human lung epithelial cells via a NADP(H) oxidase/NOX4 redox-dependent mechanism [J].