Role of ubiquitination in Na,K-ATPase regulation during lung injury

Iiro T. Helenius, Laura A. Dada, Jacob I. Sznajder

Research output: Contribution to journalReview articlepeer-review

27 Scopus citations


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,KATPase 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.

Original languageEnglish (US)
Pages (from-to)65-70
Number of pages6
JournalProceedings of the American Thoracic Society
Issue number1
StatePublished - Feb 15 2010


  • Lysosome
  • Proteasome
  • Protein degradation

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine


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