急性呼吸窘迫综合征
肺纤维化
线粒体
慢性阻塞性肺病
医学
疾病
线粒体融合
线粒体分裂
支气管肺发育不良
肺
肺动脉高压
生物信息学
线粒体DNA
生物
癌症研究
纤维化
病理
内科学
细胞生物学
遗传学
怀孕
基因
胎龄
作者
Hui Li,Xuwen Dai,Jinghua Zhou,Yujuan Wang,Shiying Zhang,Jiacheng Guo,Lidu Shen,Hengxiu Yan,Huiling Jiang
摘要
Abstract Mitochondria are dynamic organelles that continuously undergo fusion/fission to maintain normal cell physiological activities and energy metabolism. When mitochondrial dynamics is unbalanced, mitochondrial homeostasis is broken, thus damaging mitochondrial function. Accumulating evidence demonstrates that impairment in mitochondrial dynamics leads to lung tissue injury and pulmonary disease progression in a variety of disease models, including inflammatory responses, apoptosis, and barrier breakdown, and that the role of mitochondrial dynamics varies among pulmonary diseases. These findings suggest that modulation of mitochondrial dynamics may be considered as a valid therapeutic strategy in pulmonary diseases. In this review, we discuss the current evidence on the role of mitochondrial dynamics in pulmonary diseases, with a particular focus on its underlying mechanisms in the development of acute lung injury (ALI)/acute respiratory distress syndrome (ARDS), chronic obstructive pulmonary disease (COPD), asthma, pulmonary fibrosis (PF), pulmonary arterial hypertension (PAH), lung cancer and bronchopulmonary dysplasia (BPD), and outline effective drugs targeting mitochondrial dynamics‐related proteins, highlighting the great potential of targeting mitochondrial dynamics in the treatment of pulmonary disease.
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