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.
摘要：
线粒体是动态的细胞器,其持续经历融合/裂变以维持正常的细胞生理活动和能量代谢。当线粒体动力学不平衡时，线粒体稳态被打破，从而损害线粒体功能。越来越多的证据表明，线粒体动力学受损导致多种疾病模型的肺组织损伤和肺部疾病进展，包括炎症反应，凋亡，和屏障击穿，线粒体动力学的作用因肺部疾病而异。这些发现表明，线粒体动力学的调节可能被认为是肺部疾病的有效治疗策略。在这次审查中,我们讨论了线粒体动力学在肺部疾病中的作用，特别关注其在急性肺损伤（ALI）/急性呼吸窘迫综合征（ARDS）发展中的潜在机制，慢性阻塞性肺疾病(COPD),哮喘,肺纤维化（PF），肺动脉高压（PAH），肺癌和支气管肺发育不良（BPD），并概述了针对线粒体动力学相关蛋白的有效药物，强调了靶向线粒体动力学在肺部疾病治疗中的巨大潜力。
