线粒体功能障碍和生物治疗:类风湿关节炎的新研究

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引用次数: 1

摘要

观察到对线粒体及其在各种免疫介导疾病发病机制中的含义的兴趣显著增加。大量研究证实线粒体功能障碍及其病理生理后遗症是类风湿关节炎发展的关键因素。氧化应激和线粒体分子释放到细胞内和细胞外室是线粒体功能和完整性丧失的结果。一些准确反映类风湿关节炎患者氧化应激状态的生物标志物已被成功鉴定。研究人员分析了生物DMARDs (bDMARDs)治疗后这些标志物水平的变化。然而,关于靶合成DMARDs (tsDMARDs)对氧化应激的影响,目前还没有足够的数据。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Mitochondrial dysfunction and biological therapy: a new look at rheumatoid arthritis
A marked increase in interest towards the mitochondria and their implication into the pathogenesis of various immune-mediated diseases is observed. A multitude of studies are establishing the mitochondrial dysfunction and it's pathophysiological sequelae as key events, contributing to the progression of rheumatoid arthritis. The oxidative stress and release of mitochondrial molecules into the intra- and extracelular compartments are a result of the loss of function and integrity of the mitochondria. Some biomarkers, which accurately reflect the state of oxidative stress in rheumatoid arthritis patients, have been successfuly identified. The change in the levels of those markers as a result of treatment with biologic DMARDs (bDMARDs) has been analyzed. However, there is still insufficient data regarding the effect of the target-synthetic DMARDs (tsDMARDs) on the oxidative stress.
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