Research advances on the role of Na +-K +-ATPase regulation in pulmonary edema clearance of acute respiratory distress syndrome
10.3760/cma.j.cn121430-20200724-00542
- VernacularTitle:钠泵调节在急性呼吸窘迫综合征肺水清除中作用的研究进展
- Author:
Xupeng WEN
1
;
Qiquan WAN
Author Information
1. 中南大学湘雅三医院移植中心监护室，湖南长沙 410013
- Keywords:
Acute respiratory distress syndrome;
Na +-K +-ATPase;
Pulmonary edema clearance;
Long-term regulatory;
Pathway
- From:
Chinese Critical Care Medicine
2021;33(8):1011-1016
- CountryChina
- Language:Chinese
-
Abstract:
Acute respiratory distress syndrome (ARDS) is a critical disease with high mortality, and currently there is no specific treatment. ARDS is characterized by refractory hypoxemia secondary to pulmonary edema, but the underlying mechanism is not yet fully understood. Alveolar edema fluid is mainly actively transported and reabsorbed by sodium-water transport system. The sodium pump (Na +-K +-ATPase-mediated Na + transport) on the basal side of type Ⅱ alveolar epithelial cells (ATⅡ) is the main driving force for pulmonary edema clearance. Na +-K +-ATPase regulation is affected by many regulatory factors through a variety of ways, among which "long-term regulation" mechanism plays an important role, including positively regulating the gene transcription and protein expression of Na +-K +-ATPase. Na +-K +-ATPase can also be degraded by ubiquitin-proteasome pathway (UPP) and autophagy lysosome pathway to affect its abundance and enzyme activity, meanwhile, Na +-K +-ATPase α1 plays a key role in sodium water transport. We review the "long-term regulation" mechanism of Na +-K +-ATPase related pathways in pulmonary edema clearance and explore the possibility of new therapies for ARDS based on this mechanism, so as to provide new targets for the treatment of ARDS.
