Targeted interception of signaling reactive oxygen species in the vascular endothelium.
Targeted interception of signaling reactive oxygen species in the vascular endothelium.
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DOI：
10.4155/tde.11.151
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发表时间：
2012-02
影响因子：
4.2
通讯作者：
Muzykantov VR
中科院分区：
文献类型：
--
作者：
Han J;Shuvaev VV;Muzykantov VR
活性氧（ROS）是人类疾病的有害物质，也是炎症、高氧、缺血-再灌注和急性肺损伤的信号分子。由内皮细胞产生的ROS在血管病理学中起重要作用。例如，它们抑制一氧化氮，并介导促炎信号。针对血管内皮的抗氧化干预可能有助于控制这些机制。动物研究已经证明了靶向ROS-猝灭酶过氧化氢酶和超氧化物歧化酶对内皮细胞的优越性超过非靶向制剂。在过去十年中设计的多种靶向抗氧化剂制剂显示出特异性淬灭内皮ROS的有希望的结果。除了减轻过量ROS的毒性作用外，这些靶向干预还抑制促炎机制，包括内皮细胞因子活化和屏障破坏。这些干预措施可能在实验生物医学中有用，也许在转化医学中有用。
Reactive oxygen species (ROS) are implicated as injurious and as signaling agents in human maladies including inflammation, hyperoxia, ischemia-reperfusion and acute lung injury. ROS produced by the endothelium play an important role in vascular pathology. They quench, for example, nitric oxide, and mediate pro-inflammatory signaling. Antioxidant interventions targeted for the vascular endothelium may help to control these mechanisms. Animal studies have demonstrated superiority of targeting ROS-quenching enzymes catalase and superoxide dismutase to endothelial cells over nontargeted formulations. A diverse arsenal of targeted antioxidant formulations devised in the last decade shows promising results for specific quenching of endothelial ROS. In addition to alleviation of toxic effects of excessive ROS, these targeted interventions suppress pro-inflammatory mechanisms, including endothelial cytokine activation and barrier disruption. These interventions may prove useful in experimental biomedicine and, perhaps, in translational medicine.