New tricks from an old dog: mitochondrial redox signaling in cellular inflammation.
New tricks from an old dog: mitochondrial redox signaling in cellular inflammation.
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DOI：
10.1016/j.smim.2013.01.002
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发表时间：
2012-12
影响因子：
7.8
通讯作者：
Siegel RM
中科院分区：
文献类型：
--
作者：
Pelletier M;Lepow TS;Billingham LK;Murphy MP;Siegel RM
活性氧（ROS），如超氧化物（O2-）和过氧化氢（H2 O2）长期以来一直被认为是促炎性物质，但ROS的来源及其增强炎症的分子机制尚不清楚。最近的进展，在理解的先天免疫系统介导的炎症的分子基础，使这些问题被重新审视。尽管Nox 2 NADPH氧化酶产生大量ROS用于抗微生物宿主防御，但最近的研究发现，NADPH氧化酶依赖性ROS产生实际上可以抑制巨噬细胞对无菌促炎刺激的炎症反应。相反，线粒体ROS的产生已经成为宿主防御和无菌炎症的重要因素。过量的线粒体ROS可以通过呼吸链的损伤或通过线粒体功能的改变（例如增加膜电位和减少呼吸电子载体的那些）产生。在自身炎性疾病中，先天免疫应答的关键组分被基因突变或环境刺激激活，已发现炎症对线粒体ROS产生的抑制特别敏感。这些发现突出了线粒体ROS作为促炎性ROS的新发生器和炎性疾病的潜在治疗靶点。
Reactive oxygen species (ROS) such as superoxide (O2−) and hydrogen peroxide (H2O2) have long been implicated as pro-inflammatory, yet the sources of ROS and the molecular mechanisms by which they enhance inflammation have been less clear. Recent advances in the understanding of the molecular basis of inflammation mediated by the innate immune system have allowed these issues to be revisited. Although the Nox2 NADPH oxidases generate the bulk of ROS for antimicrobial host defense, recent studies have found that NADPH oxidase-dependent ROS production can actually dampen macrophage inflammatory responses to sterile pro-inflammatory stimuli. Instead, production of mitochondrial ROS has emerged as an important factor in both host defense and sterile inflammation. Excess mitochondrial ROS can be generated by either damage to the respiratory chain or by alterations of mitochondrial function such as those that increase membrane potential and reduce respiratory electron carriers. In autoinflammatory diseases, where key components of innate immune responses are activated by genetic mutations or environmental stimuli, inflammation has been found to be particularly sensitive to inhibition of mitochondrial ROS production. These findings have highlighted mitochondrial ROS as a novel generator of pro-inflammatory ROS and a potential therapeutic target in inflammatory diseases.
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影响因子：
5.3
作者：
Coant, Nicolas;Ben Mkaddem, Sanae;Ogier-Denis, Eric
通讯作者：
Ogier-Denis, Eric
影响因子：
4
作者：
Arnoult, Damien;Soares, Fraser;Girardin, Stephen E.
通讯作者：
Girardin, Stephen E.
影响因子：
4.1
作者：
Emre, Yalin;Hurtaud, Corinne;Cassard-Doulcier, Anne-Marie
通讯作者：
Cassard-Doulcier, Anne-Marie
DOI：
10.1084/jem.20102049
发表时间：
2011-03-14
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Bulua AC;Simon A;Maddipati R;Pelletier M;Park H;Kim KY;Sack MN;Kastner DL;Siegel RM
通讯作者：
Siegel RM
影响因子：
20.3
作者：
Doughty, Cheryl A.;Bleiman, Blair F.;Chiles, Thomas C.
通讯作者：
Chiles, Thomas C.