COVID-19 and Liquid Homeostasis in the Lung-A Perspective through the Epithelial Sodium Channel (ENaC) Lens.
COVID-19
SARS-CoV-2
airway liquid
alveolar liquid
epithelial Na+ channel
proteases
proteolytic cleavage
transepithelial ion transport
Journal
Cells
ISSN: 2073-4409
Titre abrégé: Cells
Pays: Switzerland
ID NLM: 101600052
Informations de publication
Date de publication:
31 05 2022
31 05 2022
Historique:
received:
03
05
2022
revised:
23
05
2022
accepted:
25
05
2022
entrez:
10
6
2022
pubmed:
11
6
2022
medline:
14
6
2022
Statut:
epublish
Résumé
Infections with a new corona virus in 2019 lead to the definition of a new disease known as Corona Virus Disease 2019 (COVID-19). The sever cases of COVID-19 and the main cause of death due to virus infection are attributed to respiratory distress. This is associated with the formation of pulmonary oedema that impairs blood oxygenation and hypoxemia as main symptoms of respiratory distress. An important player for the maintenance of a defined liquid environment in lungs needed for normal lung function is the epithelial sodium channel (ENaC). The present article reviews the implications of SARS-CoV-2 infections from the perspective of impaired function of ENaC. The rationale for this perspective is derived from the recognition that viral spike protein and ENaC share a common proteolytic cleavage site. This cleavage site is utilized by the protease furin, that is essential for ENaC activity. Furin cleavage of spike 'activates' the virus protein to enable binding to host cell membrane receptors and initiate cell infection. Based on the importance of proteolytic cleavage for ENaC function and activation of spike, it seems feasible to assume that virus infections are associated with impaired ENaC activity. This is further supported by symptoms of COVID-19 that are reminiscent of impaired ENaC function in the respiratory tract.
Identifiants
pubmed: 35681496
pii: cells11111801
doi: 10.3390/cells11111801
pmc: PMC9180030
pii:
doi:
Substances chimiques
Epithelial Sodium Channels
0
Viral Proteins
0
Peptide Hydrolases
EC 3.4.-
Furin
EC 3.4.21.75
Types de publication
Journal Article
Review
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
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