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首页> 外文期刊>Current topics in membranes >Regulation of Na,K-ATPase by Reactive Oxygen Species
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Regulation of Na,K-ATPase by Reactive Oxygen Species

机译:活性氧对Na,K-ATPase的调节

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Pulmonary edema occurs in patients with acute respiratory distress syndrome(ARDS) and congestive heart failure. Effective edema clearance is critical forthese patients to survive. The edema clearance is carried out mostly by the coor-dination of the apical Na+ channels and the basolateral Na,K-ATPase effecting ac-tive Na+ transport. Downregulation of Na+ transport occurs frequently in ARDSpatients and results in impaired edema clearance. Hypoxia, hyperoxia, particu-late matter and thrombin inhibit edema clearance. Reactive oxygen species (ROS)generated from the electron transport chain in the mitochondria and/or NADPHoxidase appears to be critical for the impaired edema clearance under these stressconditions. During hypoxia, ROS activate PKCζ , which in turn phosphorylatesNa,K-ATPase al subunit at Ser-18, leading to the endocytosis of Na,K-ATPasefrom the plasma membrane. The endocytosis of Na,K-ATPase results in decreased
机译:患有急性呼吸窘迫综合征(ARDS)和充血性心力衰竭的患者会发生肺水肿。有效的水肿清除是危重病人的生存之道。水肿清除主要是通过根尖的Na +通道和影响活性Na +转运的基底外侧Na,K-ATPase的配位来进行的。 NaDS转运的下调在ARDS患者中经常发生,并导致水肿清除功能受损。低氧,高氧,微粒物质和凝血酶抑制水肿清除。从线粒体中的电子传输链和/或NADPH氧化酶中产生的活性氧(ROS)对于在这些压力条件下受损的水肿清除而言似乎至关重要。在缺氧期间,ROS激活PKCζ,继而磷酸化Ser-18处的Na,K-ATPase al亚基,导致质膜内吞Na,K-ATPase。 Na,K-ATPase的内吞作用导致

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