线粒体功能障碍在慢性阻塞性肺疾病发病机制中的研究进展

Research progress of mitochondrial dysfunction in the pathogenesis of chronic obstructive pulmonary disease

慢性阻塞性肺疾病(COPD)是一种常见的以持续气流受限为特征的可以预防和治疗的疾病,其发病机制涉及多种细胞过程,包括氧化应激、炎症反应和蛋白酶-抗蛋白酶失衡等。线粒体是重要的细胞器,对能量的产生、维持细胞代谢、钙稳态、细胞内信号传导和细胞死亡程序的调节至关重要。线粒体功能障碍表现为线粒体活性氧生成增加、线粒体DNA损伤和异常有丝分裂。越来越多的证据表明,线粒体功能障碍在包括COPD在内的许多人类疾病的发生发展中起着重要作用。本篇综述旨在探讨线粒体功能障碍在COPD发生发展过程中的作用,以期通过靶向功能障碍的线粒体为COPD提供潜在的治疗方法。

Chronic obstructive pulmonary disease(COPD)is a common preventable and treatable disease characterized by continuous airflow restriction.The pathogenesis of COPD involves multiple cellular processes,including oxidative stress,inflammatory response,and protease-antiprotease imbalance.Mitochondrion is an important organelle which is essential for energy production,maintenance of cell metabolism,calcium homeostasis,intracellular signaling,and regulation of cell death programs.Mitochondrial dysfunction is characterized by increased production of mitochondrial reactive oxygen species,mitochondrial DNA damage and abnormal mitosis.Accumulating evidence suggests that mitochondrial dysfunction plays an important role in the occurrence and development of CODP and many other human diseases.This review aims to explore the role of mitochondrial dysfunction in the development and progression of COPD,and to provide potential therapies for COPD by targeting dysfunctional mitochondria.