氧化应激在特发性肺纤维化中的作用及其机制研究进展

The role and mechanisms of oxidative stress in idiopathic pulmonary fibrosis

特发性肺纤维化(idiopathic pulmonary fibrosis,IPF)是以弥漫性肺泡炎和成纤维细胞病理性增生最终导致肺间质纤维化为病理特征的慢性进展性疾病。IPF发病机制尚未完全明确。成肌纤维细胞(myofibroblast)增多是目前学术界认为最为重要的IPF发生致病的主要机制。同时氧化/抗氧化失衡引起的氧化应激反应是其发病重要机制之一。纠正体内氧化/抗氧化失衡能减轻肺纤维化的程度,因此有望成为治疗特发性肺纤维化的一种新方法。该文就近年来氧化应激反应在IPF中的作用及其机制研究进展作一综述。

Idiopathic pulmonary fibrosis（IPF） is an interstitial lung disease characterized by progressive pulmonary interstitial fibrosis.The pathogenesis is thought to involve abnormal reepithelialization and detuning remodeling of the extracellular matrix after alveolar injury.The increase of myofibroblast is the most important pathogenesis of IPF.At the same time oxidative stress plays a important role in many processes involved in alveolar epithelial cell injury and fibrosis.The study of oxidative stress can provide insights into pathogenesis and the discovery of new treatments.So we review the role and mechanism of oxidative stress in IPF.