Department of Medicine, Surgery and Neurosciences, Respiratory Diseases and Lung Transplant Unit, University of Siena, Viale Bracci, 16, 53100, Siena, Italy.
Hannover Medical School, Hannover University, Hannover, Germany.
Inflammation. 2020 Feb;43(1):1-7. doi: 10.1007/s10753-019-01059-1.
Idiopathic pulmonary fibrosis is characterised by abnormal reepithelialisation and remodelling consequent to persistent stimuli or injury. The involvement of oxidative stress in alveolar injury, inflammation and fibrosis development has been suggested. Increased concentrations of lipid peroxidation products, oxidised proteins and an altered antioxidant enzyme status with the depletion of glutathione, the most abundant low-molecular-weight antioxidant, have often been reported in epithelial lining fluid of IPF patients. This review describes the sources of free radical generation, ROS-induced signalling pathways and mechanisms of oxidative stress damages in the pathogenesis of idiopathic pulmonary fibrosis.
特发性肺纤维化的特征是持续的刺激或损伤导致异常的再上皮化和重塑。氧化应激在肺泡损伤、炎症和纤维化发展中的作用已被提出。在特发性肺纤维化患者的肺泡灌洗液中，常报道脂质过氧化产物、氧化蛋白浓度增加以及抗氧化酶状态改变，谷胱甘肽耗竭，谷胱甘肽是最丰富的低分子量抗氧化剂。本综述描述了自由基生成的来源、ROS 诱导的信号通路以及氧化应激损伤在特发性肺纤维化发病机制中的机制。
