Oxidative stress and pulmonary fibrosis

Article ID	Journal	Published Year	Pages	File Type
8260939	Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease	2013	13 Pages	PDF

Abstract

âº Oxidative stress is an important mechanism underlying fibrosis. âº ROS derived from the mitochondria and NOX4 can promote fibrosis. âº AEC apoptosis in lung fibrosis is coupled with mitochondria, ER, and p53 activation. âº ROS-induced AEC apoptosis is blocked in cells overexpressing Ogg1 or ACO2. âº The interactive effects between oxidative stress and TGF-Î² augment fibrosis.

Keywords

ECM AEC NOX4 XBP1 UPR ΔΨm IL-1β αSMA PKCδ AT2 NOS ERK IPF NAC Nrf2 SP-C EGFR ACO2 TNFα Alveolar epithelial type II TGF-β Jnk c-Jun N-terminal kinase Mitochondrial DNA IRE1α Mdm2 NOx O2−ROS α smooth muscle actin Hydrogen peroxide Mitochondrial aconitase NADPH oxidase Interleukin-1 beta BALF Epithelium Transforming Growth Factor Beta tumor necrosis factor-alpha EMT Apoptosis mtDNA SOD alveolar epithelial cell Superoxide Superoxide dismutase antioxidant response element nuclear factor erythroid 2-related factor 2 idiopathic pulmonary fibrosis SERCA Extracellular matrix Alveolar macrophage Bronchoalveolar lavage fluid Mitochondria nitric oxide synthase N-acetyl cysteine ARE H2O2 Unfolded protein response Mitochondrial membrane potential X-box binding protein 1 surfactant protein C Protein Kinase C Delta extracellular-signal-regulated kinase Epithelial–mesenchymal transition Reactive oxygen species Epidermal growth factor receptor