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急性肺损伤(ALI)/急性呼吸窘迫综合征(ARDS)是危重患者呼吸衰竭的常见原因，全世界重症监护病房患者中约10%会发生ARDS。尽管目前有所改善，但仍缺乏明确有效的治疗方案，死亡率依然高达30%～40%。ALI/ARDS是由炎症细胞浸润导致严重的肺泡上皮和肺泡毛细血管膜损伤、血管通透性增加、肺间质/肺泡水肿的急性炎症性过程。ARDS的病理生理学涉及多种机制，包括炎症细胞浸润、氧化应激、肺泡毛细血管屏障破坏/通透性改变、细胞凋亡和组织纤维化，涉及到MAPK、NF-κB、AMPK/SIRT1、PI3K/Akt、Nrf2/HO-1、Fas/FasL、Wnt/β-catenin、Notch等多种分子信号通路的激活。本文将对ALI发生、发展以及治疗相关分子机制的研究进展进行综述，为后续的临床与基础研究提供一定的参考。“,”Acute lung injury (ALI)/ acute respiratory distress syndrome (ARDS) is a common cause of respiratory failure in critically ill patients.ARDS occurs in about 10% of patients in intensive care units worldwide.Although the current situation has improved, there is still a lack of clear and effective treatments, and mortality and morbidity of ARDS are still as high as 30%-40%.ALI/ARDS is an acute inflammatory process caused by inflammatory cell infiltration leading to severe alveolar epithelial and alveolar capillary membrane damage, increased vascular permeability, pulmonary interstitial/alveolar edema.The pathophysiology of ARDS involves a variety of mechanisms including inflammatory cell infiltration, oxidative stress, alveolar capillary barrier disruption/permeability changes, apoptosis and tissue fibrosis, and activation of various molecular signal pathways including MAPK, NF-κB, AMPK/SIRT1, PI3K/Akt, Nrf2/HO-1, Fas/FasL, Wnt/β-catenin and Notch.This article reviews the research progress of molecular mechanisms related to the occurrence, development and treatment of ALI, in order to provide a certain reference for subsequent clinical and basic researches.