Redox signalling and the inflammatory response in rheumatoid arthritis
Redox signalling and the inflammatory response in rheumatoid arthritis
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DOI：
10.1111/j.1365-2249.2008.03634.x
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发表时间：
2008-06-01
影响因子：
4.6
通讯作者：
Xavier, R. M.
中科院分区：
文献类型：
--
作者：
Filippin, L. I.;Vercelino, R.;Xavier, R. M.
活性氧（Reactive oxygen species， ROS）主要在氧化磷酸化和氧化爆发过程中由活化的吞噬细胞产生。ROS的过量产生会损害脂质、蛋白质、膜和核酸。它们也作为重要的细胞内信号，增强炎症反应。许多研究表明，ROS在炎性慢性关节病（如类风湿关节炎）的发病机制中起作用。众所周知，ROS可以作为激活核因子kappa-B的第二信使，该因子协调炎症反应中一系列基因的表达。因此，了解这些途径之间复杂的相互作用可能有助于开发新的类风湿关节炎治疗策略。
Reactive oxygen species (ROS) are produced mainly during oxidative phosphorylation and by activated phagocytic cells during oxidative burst. The excessive production of ROS can damage lipids, protein, membrane and nucleic acids. They also serve as important intracellular signalling that enhances the inflammatory response. Many studies have demonstrated a role of ROS in the pathogenesis of inflammatory chronic arthropathies, such as rheumatoid arthritis. It is known that ROS can function as a second messenger to activate nuclear factor kappa-B, which orchestrates the expression of a spectrum of genes involved in the inflammatory response. Therefore, an understanding of the complex interactions between these pathways might be useful for the development of novel therapeutic strategies for rheumatoid arthritis.