Hyperoxia-induced signal transduction pathways in pulmonary epithelial cells.
Hyperoxia-induced signal transduction pathways in pulmonary epithelial cells.
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DOI：
10.1016/j.freeradbiomed.2007.01.021
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发表时间：
2007-04
影响因子：
7.4
通讯作者：
T. E. Zaher;E. Miller;Dympna M. P. Morrow;M. Javdan;L. Mantell
中科院分区：
文献类型：
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作者：
T. E. Zaher;E. Miller;Dympna M. P. Morrow;M. Javdan;L. Mantell
高氧机械通气对于治疗重症患者是必要的。然而，长时间暴露于高氧导致产生过量的活性氧（ROS），这可引起急性炎性肺损伤。高氧的主要影响之一是肺上皮的损伤和死亡，这伴随着肺促炎细胞因子水平的增加和过度的白细胞浸润。深入了解导致肺上皮细胞损伤/死亡的信号通路可能有助于深入了解高氧诱导的急性炎症性肺损伤的发病机制。本文综述了上皮细胞对高氧的反应，上皮细胞损伤/死亡的主要调控因素，以及高氧暴露后的促炎反应。我们详细讨论了一些最有趣的球员，如NF-κB，可以调节促炎反应和细胞损伤/死亡的肺上皮细胞。更好地了解这些因子的功能无疑将有助于我们描绘高氧细胞死亡和促炎反应的途径。
Mechanical ventilation with hyperoxia is necessary to treat critically ill patients. However, prolonged exposure to hyperoxia leads to the generation of excessive reactive oxygen species (ROS), which can cause acute inflammatory lung injury. One of the major effects of hyperoxia is the injury and death of pulmonary epithelium, which is accompanied by increased levels of pulmonary proinflammatory cytokines and excessive leukocyte infiltration. A thorough understanding of the signaling pathways leading to pulmonary epithelial cell injury/death may provide some insights into the pathogenesis of hyperoxia-induced acute inflammatory lung injury. This review focuses on epithelial responses to hyperoxia and some of the major factors regulating pathways to epithelial cell injury/death, and proinflammatory responses on exposure to hyperoxia. We discuss in detail some of the most interesting players, such as NF-κB, that can modulate both proinflammatory responses and cell injury/death of lung epithelial cells. A better appreciation for the functions of these factors will no doubt help us to delineate the pathways to hyperoxic cell death and proinflammatory responses.