线粒体自噬与高原肺水肿相关性研究进展

Research Progress on the Relationship between Mitochondrial Autophagy and High Altitude Pulmonary Edema

高原肺水肿(high altitude pulmonary edema, HAPE)是指当平原或较低海拔的人们快速进入2500 m以上的高原,因缺氧无法供应机体需求从而导致的一种非心源性肺水肿,其发病机制目前认为与肺泡或肺间质出现大量肺血管内的液体,造成肺血容量增多,肺血管收缩、肺动脉压力升高、肺毛细血管通透性增加以及肺泡II型上皮细胞液体清除能力下降等因素有关。近年研究结果提示,患有高原肺水肿人群在缺氧条件下,机体内活性氧(reactive oxygen species, ROS)大量生成,线粒体随之发生功能障碍而引起自噬。文章将以线粒体自噬与高原肺水肿的相关性分析进行研究综述,从线粒体自噬参与高原肺水肿的发生机制提供理论依据。

High altitude pulmonary edema (HAPE) refers to a type of non-cardiogenic pulmonary edema that occurs when people in the plains or lower altitudes quickly enter the plateau above 2500 m due to lack of oxygen to supply the body’s needs. Pathogenesis is currently believed to be related to the presence of a large amount of pulmonary fluid in the alveoli or pulmonary interstitium, resulting in increased pulmonary blood volume, pulmonary vasoconstriction, increased pulmonary artery pressure, increased pulmonary capillary permeability, and decreased liquid clearance of alveolar type II epithelial cells and other factors. Recent research results suggest that in people with high altitude pulmonary edema, reactive oxygen species (ROS) are produced in large quantities in the body under hypoxic conditions, and mitochondrial dysfunction will cause autophagy. This article will review the research on the correlation between mitochondrial autophagy and high altitude pulmonary edema, and provide a theoretical basis from the mechanism of mitochondrial autophagy participating in the occurrence of high altitude pulmonary edema.