Liu Jian-Yu, Zhang Meng-Yu, Qu Yi-Qing
Department of Pulmonary and Critical Care Medicine, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, People's Republic of China.
Department of Pulmonary and Critical Care Medicine, Qilu Hospital of Shandong University, Jinan, Shandong, People's Republic of China.
Int J Chron Obstruct Pulmon Dis. 2020 Sep 15;15:2167-2177. doi: 10.2147/COPD.S265728. eCollection 2020.
COPD is a common disease of the respiratory system. Inflammation, cellular senescence and necroptosis are all pathological alterations of this disease, which may lead to emphysema and infection that aggravate disease progression. Mitochondria acting as respiration-related organelles is usually observed with abnormal changes in morphology and function in CS-stimulated models and COPD patients. Damaged mitochondria can activate mitophagy, a vital mechanism for mitochondrial quality control, whereas under the persistent stimulus of CS or other forms of oxidative stress, mitophagy is impaired, resulting in insufficient clearance of damaged mitochondria. However, the excessive activation of mitophagy also seems to disturb the pathology of COPD. In this review, we demonstrate the variations in mitochondria and mitophagy in CS-induced models and COPD patients and discuss the underlying regulatory mechanism of mitophagy and COPD, including the roles of inflammation, senescence, emphysema and infection.
慢性阻塞性肺疾病（COPD）是一种常见的呼吸系统疾病。炎症、细胞衰老和坏死性凋亡都是该疾病的病理改变，可能导致肺气肿和感染，从而加重疾病进展。线粒体作为与呼吸相关的细胞器，在香烟烟雾（CS）刺激模型和COPD患者中通常观察到其形态和功能发生异常变化。受损的线粒体可激活线粒体自噬，这是线粒体质量控制的重要机制，而在CS或其他形式氧化应激的持续刺激下，线粒体自噬受损，导致受损线粒体清除不足。然而，线粒体自噬的过度激活似乎也会扰乱COPD的病理过程。在本综述中，我们展示了CS诱导模型和COPD患者中线粒体和线粒体自噬的变化，并讨论了线粒体自噬与COPD的潜在调控机制，包括炎症、衰老、肺气肿和感染的作用。
