Liu Danjuan, Weng Shuoyun, Fu Chunjin, Guo Rongjie, Chen Min, Shi Bingbing, Weng Junting
Department of Critical Care Medicine, the Affiliated Hospital of Putian University, Putian, 351100, China.
School of Optometry and Ophthalmology, Wenzhou Medical University, Wenzhou, China.
Cell Biochem Biophys. 2025 Jun;83(2):1415-1425. doi: 10.1007/s12013-024-01604-2. Epub 2024 Nov 11.
Acute lung injury (ALI) is a critical condition marked by rapid-onset respiratory failure due to extensive inflammation and increased pulmonary vascular permeability, often progressing to acute respiratory distress syndrome (ARDS) with high mortality. Autophagy, a cellular degradation process essential for removing damaged organelles and proteins, plays a crucial role in regulating lung injury and repair. This review examines the protective role of autophagy in maintaining cellular function and reducing inflammation and oxidative stress in ALI. It underscores the necessity of precise regulation to fully harness the therapeutic potential of autophagy in this context. We summarize the mechanisms by which autophagy influences lung injury and repair, discuss the interplay between autophagy and apoptosis, and examine potential therapeutic strategies, including autophagy inducers, targeted autophagy signaling pathways, antioxidants, anti-inflammatory drugs, gene editing, and stem cell therapy. Understanding the role of autophagy in ALI could lead to novel interventions for improving patient outcomes and reducing mortality rates associated with this severe condition.
急性肺损伤（ALI）是一种危急病症，其特征为因广泛炎症和肺血管通透性增加而迅速发生呼吸衰竭，常进展为急性呼吸窘迫综合征（ARDS），死亡率很高。自噬是一种清除受损细胞器和蛋白质所必需的细胞降解过程，在调节肺损伤和修复中起关键作用。本综述探讨了自噬在维持细胞功能以及减轻ALI中的炎症和氧化应激方面的保护作用。强调了精确调控的必要性，以便在这种情况下充分发挥自噬的治疗潜力。我们总结了自噬影响肺损伤和修复的机制，讨论了自噬与细胞凋亡之间的相互作用，并研究了潜在的治疗策略，包括自噬诱导剂、靶向自噬信号通路、抗氧化剂、抗炎药物、基因编辑和干细胞治疗。了解自噬在ALI中的作用可能会带来新的干预措施，以改善患者预后并降低与这种严重病症相关的死亡率。
