Oxidative Stress in COPD: Sources, Markers, and Potential Mechanisms.
Oxidative Stress in COPD: Sources, Markers, and Potential Mechanisms.
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DOI：
10.3390/jcm6020021
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发表时间：
2017-02-15
影响因子：
3.9
通讯作者：
Sapey E
中科院分区：
文献类型：
--
作者：
McGuinness AJ;Sapey E
慢性阻塞性肺疾病（COPD）中氧化应激标志物增加，活性氧（ROS）能够改变生物分子、信号通路和抗氧化分子功能，其中许多与COPD的发病机制有关。然而，ROS参与COPD的发生和进展尚未得到证实。在这里，我们将讨论活性氧的来源，以及为防止其有害影响而进化出的防御机制。我们讨论了ROS在COPD的发展和进展中可能发挥的作用，以及目前限制其造成的损害的治疗尝试。有证据表明，COPD患者的几个关键细胞的功能出现改变，重要的氧化剂和抗氧化分子的表达水平可能异常。试图恢复这些分子平衡的治疗试验并没有对疾病的所有方面产生影响，尽管ROS影响COPD的理论似乎是合理的，但目前测试组织损伤相关途径的模型是有限的。COPD患者的异质性对我们的理解提出了挑战，需要进一步的研究来确定潜在的靶点和分层的COPD患者人群，在这些人群中ROS治疗可能是最有效的。
Markers of oxidative stress are increased in chronic obstructive pulmonary disease (COPD) and reactive oxygen species (ROS) are able to alter biological molecules, signaling pathways and antioxidant molecule function, many of which have been implicated in the pathogenesis of COPD. However, the involvement of ROS in the development and progression of COPD is not proven. Here, we discuss the sources of ROS, and the defences that have evolved to protect against their harmful effects. We address the role that ROS may have in the development and progression of COPD, as well as current therapeutic attempts at limiting the damage they cause. Evidence has indicated that the function of several key cells appears altered in COPD patients, and expression levels of important oxidant and antioxidant molecules may be abnormal. Therapeutic trials attempting to restore equilibrium to these molecules have not impacted upon all facets of disease and whilst the theory behind ROS influence in COPD appears sound, current models testing relevant pathways to tissue damage are limited. The heterogeneity seen in COPD patients presents a challenge to our understanding, and further research is essential to identify potential targets and stratified COPD patient populations where ROS therapies may be maximally efficacious.