...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Circulation journal >Subcellular localization of oxidants and redox modulation of endothelial nitric oxide synthase
【24h】

Subcellular localization of oxidants and redox modulation of endothelial nitric oxide synthase

机译：内皮一氧化氮合酶氧化剂的亚细胞定位和氧化还原调节

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Reactive oxygen species (ROS) have long been viewed as deleterious chemicals that lead to oxidative stress. More recently, ROS, especially the stable ROS hydrogen peroxide (H2O2), have been shown to have roles in normal physiological responses in vascular cells. Endothelial nitric oxide synthase (eNOS) is dynamically targeted to plasmalemmal caveolae, and represents the principal enzymatic source of nitric oxide (NO?) in the vascular wall. eNOS maintains normal vascular tone and inhibits the clinical expression of many cardiovascular diseases. Increases in oxidative stress are associated with eNOS dysfunction. In a paradigm shift in the conceptual framework linking redox biochemistry and vascular function, H2O2 has been established as a physiological mediator in signaling pathways, yet the intracellular sources of H2O2 and their regulation remain incompletely understood. The subcellular distributions of ROS and of ROS-modified proteins critically influence the redox-sensitive regulation of eNOS-dependent pathways. ROS localization in specific subcellular compartments can lead to selective oxidative modifications of eNOS and eNOS-associated proteins. Likewise, the dynamic targeting of eNOS and other signaling proteins influences their interactions with reactive nitrogen species and ROS that are also differentially distributed within the cell. Thus, the subcellular distribution both of eNOS and redox-active biomolecules serves as a critical basis for the control of the "redox switch" that influences NO?- and oxidant-regulated signaling pathways. Here we discuss the biochemical factors, cellular determinants, and molecular mechanisms that modulate redox-sensitive regulation of eNOS and NO? signaling under normal and pathological conditions.
机译：活性氧物种（ROS）长期被视为导致氧化应激的有害化学品。最近，ROS，特别是稳定的ROS过氧化氢（H2O2），已被证明在血管细胞中正常的生理反应中具有作用。内皮型一氧化氮合酶（Enos）动态靶向plasmalemal Caveolae，并且代表血管壁中的一氧化氮（NO 2）的本金酶源。 eNOS保持正常的血管基调并抑制许多心血管疾病的临床表达。氧化应激的增加与enos功能障碍有关。在连接氧化还原生物化学和血管功能的概念框架中的范式转变中，H2O2已经建立为信号通路中的生理介质，但H2O2的细胞内来源及其调节仍然不完全理解。 ROS和ROS改性蛋白质的亚细胞分布重视依赖于依赖途径的氧化还原敏感调控。在特定的亚细胞室中的ROS定位可以导致ENOS和相关蛋白的选择性氧化修饰。同样地，eNOS和其他信号蛋白的动态靶向影响它们与反应性氮物质和RO的相互作用，这些反应性氮物质和ROS也差异地分布在细胞内。因此，eNOS和氧化还原活性生物分子的亚细胞分布是对影响NOα和氧化剂调节的信号通路的“氧化还原开关”的控制的关键基础。在这里，我们讨论了调节eNOS氧化还原敏感调节的生化因子，细胞决定因素和分子机制？正常和病理条件下的信号传导。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号