肺纤维化
线粒体
线粒体ROS
背景(考古学)
纤维化
肺
特发性肺纤维化
生物
活性氧
癌症研究
医学
免疫学
病理
细胞生物学
内科学
古生物学
作者
Jennifer L. Larson‐Casey,Chao He,A.Brent Carter
出处
期刊:Redox biology
[Elsevier]
日期:2020-06-01
卷期号:33: 101426-101426
被引量:65
标识
DOI:10.1016/j.redox.2020.101426
摘要
Mechanisms underlying the pathogenesis of pulmonary fibrosis remain incompletely understood. Emerging evidence suggests changes in mitochondrial quality control are a critical determinant in many lung diseases, including chronic obstructive pulmonary disease, asthma, pulmonary hypertension, acute lung injury, lung cancer, and in the susceptibility to pulmonary fibrosis. Once thought of as the kidney-bean shaped powerhouses of the cell, mitochondria are now known to form interconnected networks that rapidly and continuously change their size to meet cellular metabolic demands. Mitochondrial quality control modulates cell fate and homeostasis, and diminished mitochondrial quality control results in mitochondrial dysfunction, increased reactive oxygen species (ROS) production, reduced ATP production, and often induces intrinsic apoptosis. Here, we review the role of the mitochondria in alveolar epithelial cells, lung macrophages, and fibroblasts within the context of pulmonary fibrosis.
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