线粒体自噬与高氧肺损伤的研究进展

Research Progress of Mitophagy and Hyperoxic Lung Injury

氧气常被用于抢救、治疗,但长期吸入高浓度氧气可造成机体急性肺损伤,严重时还可出现呼吸窘迫和呼吸衰竭。高氧条件下,线粒体可产生过量的氧自由基,发生氧化应激,损伤肺组织,导致肺结构和功能异常,其主要途径可能为氧自由基刺激肺部细胞发生炎症反应、细胞凋亡,导致组织修复异常、肺发育受阻等。线粒体自噬可选择性清除受损的线粒体,调控线粒体质量,维持机体平衡,且线粒体自噬可能与高氧肺损伤的发生发展存在一定相关性。因此,深入了解线粒体自噬在高氧肺损伤防治中的作用机制具有重要意义。

Oxygen is often used to rescue and treatment,but long-term inhalation of high concentration of oxygen can cause acute lung injury to the body,andrespiratory distress and respiratory failure in severe cases.Under the condition of high oxygen,mitochondria can produce excessive oxygen free radicals,produce oxidative stress to damage lung tissue,and lead to abnormal lung structure and function.The main way may be oxygen radicals to stimulate lung cells inflammation,apoptosis,leading to abnormal tissue repair and blocked lung development,etc.Mitophagy can selectively remove damaged mitochondria to regulate mitochondrial quality,maintain body balance,and mitophagy may have some correlation with the occurrence and development of hyperoxic lung injury.Therefore,it is important to gain a deeper understanding of the mechanism of mitophagy in the prevention and treatment of hyperoxic lung injury.