肺泡巨噬细胞死亡方式对急性呼吸窘迫综合征作用研究进展  

Research progress on the effect of alveolar macrophage cell death pattern on acute respiratory distress syndrome

作　　者：冷雪芊 卢文斌 杨金慧 林省伟 卞金俊 Leng Xueqian;Lu Wenbin;Yang Jinhui;Lin Shengwei;Bian Jinjun(Faculty of Anesthesiology,the First Affiliated Hospital of Naval Medical University,Shanghai 200433,China)

机构地区：[1]海军军医大学第一附属医院麻醉学部,上海200433

出　　处：《国际麻醉学与复苏杂志》2024年第11期1222-1226,共5页International Journal of Anesthesiology and Resuscitation

基　　金：国家自然科学基金(82272205)。

摘　　要：急性呼吸窘迫综合征(ARDS)是由多种病理因素引起的急性炎性肺损伤, 主要临床特征为呼吸窘迫、顽固性低氧血症和呼吸衰竭, 严重影响患者的生命和健康。肺泡巨噬细胞(AM)的死亡在ARDS炎症反应中扮演了关键的调控角色。这些细胞的死亡可以影响其他免疫细胞群, 调控炎症进程, 并在细胞死亡和肺损伤之间形成增强的正反馈机制。文章综述了包括焦亡、凋亡、自噬及铁死亡在内的AM不同死亡方式的分子机制, 以及在ARDS炎症进程中产生的调节作用, 并通过近年的相关研究文献对其作用机制进行分析, 从而对未来ARDS的治疗提供新的思路。Acute respiratory distress syndrome(ARDS)is an acute inflammatory lung injury caused by various pathological factors.Its main clinical features include respiratory distress,refractory hypoxemia,and respiratory failure,which severely affect the patient's life and health.The death of alveolar macrophages(AM)plays a key regulaiory role in the inflammatory response during ARDS.The death of these cells can influence other immune cell populations,promote the progression of inflammation,and create an amplified positive feedback mechanism between cell death and lung injury.This article reviews the molecular mechanisms of various forms of AM cell death,including pyroptosis,apoptosis,autophagy,and ferroptosis,as well as their regulatory roles in the inflammatory process of ARDS.Moreover,recent research is analyzed to provide insights into the mechanisms of these processes,offering new therapeutic approaches for the future treatment of ARDS.

关 键 词：急性呼吸窘迫综合征 肺损伤 肺泡巨噬细胞 炎症反应 细胞死亡 

分 类 号：R563.8[医药卫生—呼吸系统]