Epithelial Mitochondrial Dysfunction in Lung Disease

被引:28
作者
Zhang, Linlin [1 ]
Wang, William [1 ]
Zhu, Bijun [1 ]
Wang, Xiangdong [1 ]
机构
[1] Fudan Univ, Shanghai Med Coll, Zhongshan Hosp, Inst Clin Sci, Shanghai, Peoples R China
来源
MITOCHONDRIAL DNA AND DISEASES | 2017年 / 1038卷
关键词
Mitochondria; Structure; Apoptosis; Reactive oxygen species; COPD; OBSTRUCTIVE PULMONARY-DISEASE; INTEGRATING INFLAMMATORY MEDIATORS; OXIDATIVE STRESS; CLINICAL INFORMATICS; DENDRITIC CELLS; CANCER CELLS; DNA-DAMAGE; BIOMARKERS; APOPTOSIS; GLUTATHIONE;
D O I
10.1007/978-981-10-6674-0_14
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Since the twentieth century, scientists have studied the functions and mechanisms of the mitochondria. The mitochondrion plays many important roles in cell functioning and contributes to apoptosis, embryonic and tissue development, aging, etc. Consequently, mitochondrial dysfunction often has a direct impact on health such as aging, tumorigenesis, lung injury and COPD, etc. Recent evidence indicates that the mitochondria could also be a crucial contributor to immunity with functions such as biogenesis, fusion, and fission impacting various areas in initializing immunity. In this review, we will describe both the structure and various functions of the mitochondria with an emphasis on functions such ATP production which is crucial for a multitude of processes such as apoptosis, biosynthesis of Fe/S clusters, steroid synthesis, and, more fundamentally, cell survival. In addition, this review aims to investigate the relationship of epithelial mitochondria and lung disease. Cigarette smoke is known to induce structural and functional mutations in airway epithelial mitochondria often acting as an indicator for diseases such as COPD. Further evidence to support this speculation is the presence of reactive oxygen species (ROS) within cigarette smoke which is a factor in the development of COPD.
引用
收藏
页码:201 / 217
页数:17
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