The pathophysiological role of mitochondrial oxidative stress in lung diseases.

The pathophysiological role of mitochondrial oxidative stress in lung diseases.
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线粒体氧化应激在肺部疾病中的病理生理作用

DOI:
10.1186/s12967-017-1306-5
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发表时间:
2017-10-13
影响因子:
7.4
通讯作者:
Chen Z
Chen Z
中科院分区:
医学2区
文献类型:
--
作者:
Liu X;Chen Z

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线粒体在活性氧(ROS)依赖性肺疾病如肺纤维化、石棉、慢性气道疾病和肺癌中起关键作用。线粒体DNA(mtDNA)编码线粒体蛋白质,比核DNA对氧化剂更敏感。线粒体DNA损伤导致线粒体功能障碍,包括电子传递链损伤和线粒体膜电位丧失。此外,受损的mtDNA还作为损伤相关分子模式(DAMP)驱动炎症和免疫反应。在这篇综述中,肺泡上皮细胞,肺泡巨噬细胞和线粒体之间的串扰检查。ROS相关的转录因子和下游细胞信号通路也进行了讨论。我们的结论是,靶向氧化应激与抗氧化剂,如硫醇分子,多酚和超氧化物歧化酶(SOD),并促进线粒体生物合成应被视为治疗肺部疾病,目前没有有效的治疗方案的新策略。
Mitochondria are critically involved in reactive oxygen species (ROS)-dependent lung diseases, such as lung fibrosis, asbestos, chronic airway diseases and lung cancer. Mitochondrial DNA (mtDNA) encodes mitochondrial proteins and is more sensitive to oxidants than nuclear DNA. Damage to mtDNA causes mitochondrial dysfunction, including electron transport chain impairment and mitochondrial membrane potential loss. Furthermore, damaged mtDNA also acts as a damage-associated molecular pattern (DAMP) that drives inflammatory and immune responses. In this review, crosstalk among alveolar epithelial cells, alveolar macrophages and mitochondria is examined. ROS-related transcription factors and downstream cell signaling pathways are also discussed. We conclude that targeting oxidative stress with antioxidant agents, such as thiol molecules, polyphenols and superoxide dismutase (SOD), and promoting mitochondrial biogenesis should be considered as novel strategies for treating lung diseases that currently have no effective treatment options.
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