Endoplasmic Reticulum Stress in Chronic Obstructive Pulmonary Disease: Mechanisms and Future Perspectives

被引：18

作者：

Yu, Yue ^{[1
]}

Yang, Ailin ^{[1
]}

Yu, Ganggang ^{[1
]}

Wang, Haoyan ^{[1
]}

机构：

[1] Capital Med Univ, Beijing Friendship Hosp, Dept Resp Med, Beijing 100050, Peoples R China

来源：

BIOMOLECULES | 2022年 / 12卷 / 11期

基金：

北京市自然科学基金; 中国国家自然科学基金;

关键词：

endoplasmic reticulum stress; chronic obstructive pulmonary disease; inflammation; apoptosis; autophagy; therapeutic; UNFOLDED PROTEIN RESPONSE; XBP1; MESSENGER-RNA; FACTOR-KAPPA-B; CIGARETTE-SMOKE; ER STRESS; HOMOLOGOUS PROTEIN; INDUCED AUTOPHAGY; INDEPENDENT ACTIVATION; CELLULAR SENESCENCE; ENDOTHELIAL-CELLS;

D O I：

10.3390/biom12111637

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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.

引用

页数：20

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