泛素化在肺损伤过程中对 Na,K-ATP 酶调节的作用。
Role of ubiquitination in Na,K-ATPase regulation during lung injury.
机构信息
Pulmonary and Critical Care Medicine, Feinberg School of Medicine, Northwestern University, 240 E. Huron, McGaw Pavilion M-300, Chicago, IL 60611, USA.
出版信息
Proc Am Thorac Soc. 2010 Feb;7(1):65-70. doi: 10.1513/pats.200907-082JS.
During acute lung injury edema accumulates in the alveolar space, resulting in hypoxemia due to intrapulmonary shunt. The alveolar Na,K-ATPase, by effecting active Na(+) transport, is essential for removing edema from the alveolar spaces. However, during hypoxia it is endocytosed and degraded, which results in decreased Na,K-ATPase function and impaired lung edema clearance. Na,K-ATPase endocytosis and degradation require the phosphorylation and subsequent ubiquitination of the Na,K-ATPase. These events are the results of cross-talk between post-translational modifications, and how ubiquitination of a specific protein can result from injurious extracellular stimuli. Here, we review current knowledge on the regulation of Na,K-ATPase activity during lung injury, focusing on the role of Na,K-ATPase ubiquitination during hypoxia. A better understanding of these signaling pathways can be of relevance for the design of novel treatments to ameliorate the deleterious effects of acute lung injury.
在急性肺损伤中，水肿积聚在肺泡空间中，导致由于肺内分流而出现低氧血症。肺泡 Na,K-ATP 酶通过促进主动 Na(+)转运，对于从肺泡空间中清除水肿是必不可少的。然而，在缺氧时，它会被内吞和降解，导致 Na,K-ATP 酶功能下降和肺水肿清除受损。Na,K-ATP 酶的内吞和降解需要 Na,K-ATP 酶的磷酸化和随后的泛素化。这些事件是翻译后修饰之间相互作用的结果，以及特定蛋白质的泛素化如何可以由损伤性细胞外刺激引起。在这里，我们综述了肺损伤期间 Na,K-ATP 酶活性调节的最新知识，重点介绍了缺氧期间 Na,K-ATP 酶泛素化的作用。更好地了解这些信号通路对于设计新的治疗方法来减轻急性肺损伤的有害影响可能具有重要意义。
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