内质网应激在慢性阻塞性肺疾病中的作用：机制与展望。

Department of Respiratory Medicine, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, China.

Biomolecules. 2022 Nov 4;12(11):1637. doi: 10.3390/biom12111637.

The endoplasmic reticulum (ER) is an integral organelle for maintaining protein homeostasis. Multiple factors can disrupt protein folding in the lumen of the ER, triggering ER stress and activating the unfolded protein response (UPR), which interrelates with various damage mechanisms, such as inflammation, apoptosis, and autophagy. Numerous studies have linked ER stress and UPR to the progression of chronic obstructive pulmonary disease (COPD). This review focuses on the mechanisms of other cellular processes triggered by UPR and summarizes drug intervention strategies targeting the UPR pathway in COPD to explore new therapeutic approaches and preventive measures for COPD.

内质网（ER）是维持蛋白质动态平衡的重要细胞器。多种因素可破坏内质网腔中的蛋白质折叠，触发内质网应激并激活未折叠蛋白反应（UPR），UPR 与炎症、细胞凋亡和自噬等多种损伤机制相互关联。大量研究表明，内质网应激和 UPR 与慢性阻塞性肺疾病（COPD）的进展有关。本综述重点关注 UPR 触发的其他细胞过程的机制，并总结针对 COPD 中 UPR 途径的药物干预策略，以探索 COPD 的新治疗方法和预防措施。