Linking oxidative stress to inflammation: Toll-like receptors.
Linking oxidative stress to inflammation: Toll-like receptors.
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DOI：
10.1016/j.freeradbiomed.2010.01.006
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发表时间：
2010-05-01
影响因子：
7.4
通讯作者：
Billiar, Timothy
中科院分区：
文献类型：
--
作者：
Gill, Roop;Tsung, Allan;Billiar, Timothy
关键词：
氧化应激导致的损伤发生在许多涉及缺血和再灌注的临床情况中，例如器官移植、出血性休克（HS）、心肌梗死和脑血管意外。由于细胞的氧化还原状态的干扰而导致的免疫系统的激活似乎有助于这些条件下的组织和器官损伤。氧化应激和炎症途径之间的联系知之甚少。最近，Toll样受体（TLR）已被证明介导实验性缺血和再灌注（I/R）中观察到的炎症反应。TLR家族的受体参与警告先天免疫系统的危险似乎是由损伤相关的分子模式分子（DAMP），在氧化应激条件下释放激活。在这篇综述中，我们将研究TLR在各种氧化应激实验模型中的作用，如HS和I/R。我们还将报告可能与TLR相互作用介导损伤的潜在DAMP。最后，将探讨NADPH氧化酶的活性氧通过TLR信号启动炎症通路的潜在机制。
Injury caused by oxidative stress occurs in many clinical scenarios involving ischemia and reperfusion such as organ transplantation, hemorrhagic shock (HS), myocardial infarction and cerebral vascular accidents. Activation of the immune system as a result of disturbances in the redox state of cells appears to contribute to tissue and organ damage in these conditions. The link between oxidative stress and inflammatory pathways is poorly understood. Recently, Toll like receptors (TLRs) have been shown to mediate the inflammatory response seen in experimental ischemia and reperfusion (I/R). The TLR family of receptors involved in alerting the innate immune system of danger appears to be activated by damage associated molecular pattern molecules (DAMPs) that are released during condition of oxidative stress. In this review, we will examine the role of TLRs in various experimental models of oxidative stress such as HS and I/R. We will also report on potential DAMPs that may interact with TLRs in mediating injury. Finally, potential mechanisms by which reactive oxygen species from NADPH oxidase can signal the commencement of inflammatory pathways through TLRs will be explored.
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