Molecular mechanisms of Na,K-ATPase dysregulation driving alveolar epithelial barrier failure in severe COVID-19.
Am J Physiol Lung Cell Mol Physiol
; 320(6): L1186-L1193, 2021 06 01.
Article
in English
| MEDLINE | ID: covidwho-1124630
ABSTRACT
A significant number of patients with coronavirus disease 2019 (COVID-19) develop acute respiratory distress syndrome (ARDS) that is associated with a poor outcome. The molecular mechanisms driving failure of the alveolar barrier upon severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection remain incompletely understood. The Na,K-ATPase is an adhesion molecule and a plasma membrane transporter that is critically required for proper alveolar epithelial function by both promoting barrier integrity and resolution of excess alveolar fluid, thus enabling appropriate gas exchange. However, numerous SARS-CoV-2-mediated and COVID-19-related signals directly or indirectly impair the function of the Na,K-ATPase, thereby potentially contributing to disease progression. In this Perspective, we highlight some of the putative mechanisms of SARS-CoV-2-driven dysfunction of the Na,K-ATPase, focusing on expression, maturation, and trafficking of the transporter. A therapeutic mean to selectively inhibit the maladaptive signals that impair the Na,K-ATPase upon SARS-CoV-2 infection might be effective in reestablishing the alveolar epithelial barrier and promoting alveolar fluid clearance and thus advantageous in patients with COVID-19-associated ARDS.
Keywords
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
Pulmonary Alveoli
/
Sodium-Potassium-Exchanging ATPase
/
Tight Junctions
/
Severe Acute Respiratory Syndrome
/
COVID-19
Type of study:
Prognostic study
Limits:
Humans
Language:
English
Journal:
Am J Physiol Lung Cell Mol Physiol
Journal subject:
Molecular Biology
/
Physiology
Year:
2021
Document Type:
Article
Affiliation country:
Ajplung.00056.2021
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