A key role for NOX4 in epithelial cell death during development of lung fibrosis

• Published in: Antioxidants & redox signaling Vol. 15; no. 3; p. 607
• Main Authors: Carnesecchi, Stephanie, Deffert, Christine, Donati, Yves, Basset, Olivier, Hinz, Boris, Preynat-Seauve, Olivier, Guichard, Cecile, Arbiser, Jack L, Banfi, Botond, Pache, Jean-Claude, Barazzone-Argiroffo, Constance, Krause, Karl-Heinz
• Format: Journal Article
• Language: English
• Published: United States 01.08.2011
• Subjects: Animals; Apoptosis - drug effects; Apoptosis - genetics; Bleomycin - pharmacology; Cells, Cultured; Gene Expression; Idiopathic Pulmonary Fibrosis - genetics; Idiopathic Pulmonary Fibrosis - metabolism; Idiopathic Pulmonary Fibrosis - pathology; Male; Mice; NADPH Oxidase 4; NADPH Oxidases - antagonists & inhibitors; NADPH Oxidases - genetics; NADPH Oxidases - metabolism; Oxidative Stress - genetics; Pulmonary Alveoli - drug effects; Pulmonary Alveoli - metabolism; Pulmonary Alveoli - pathology; Reactive Oxygen Species - metabolism; Respiratory Mucosa - metabolism; Respiratory Mucosa - pathology; RNA, Small Interfering - genetics; Smad2 Protein - metabolism; Transforming Growth Factor beta1 - metabolism

The pathogenesis of pulmonary fibrosis is linked to oxidative stress, possibly generated by the reactive oxygen species (ROS) generating NADPH oxidase NOX4. Epithelial cell death is a crucial early step in the development of the disease, followed only later by the fibrotic stage. We demonstrate that...