Fibrinolytic system and COVID-19: From an innovative view of epithelial ion transport.
COVID-19
Epithelial sodium channel
Fibrinolytic system
Plasmin
SARS-CoV-2
Journal
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
ISSN: 1950-6007
Titre abrégé: Biomed Pharmacother
Pays: France
ID NLM: 8213295
Informations de publication
Date de publication:
Jul 2023
Jul 2023
Historique:
received:
13
03
2023
revised:
05
05
2023
accepted:
06
05
2023
medline:
29
5
2023
pubmed:
12
5
2023
entrez:
12
5
2023
Statut:
ppublish
Résumé
Lifeways of worldwide people have changed dramatically amid the coronavirus disease 2019 (COVID-19) pandemic, and public health is at stake currently. In the early stage of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, fibrinolytic system is mostly inhibited, which is responsible for the development of hypofibrinolysis, promoting disseminated intravascular coagulation, hyaline membrane formation, and pulmonary edema. Whereas the common feature and risk factor at advanced stage is a large amount of fibrin degradation products, including D-dimer, the characteristic of hyperfibrinolysis. Plasmin can cleave both SARS-CoV-2 spike protein and γ subunit of epithelial sodium channel (ENaC), a critical element to edematous fluid clearance. In this review, we aim to sort out the role of fibrinolytic system in the pathogenesis of COVID-19, as well as provide the possible guidance in current treating methods. In addition, the abnormal regulation of ENaC in the occurrence of SARS-CoV-2 mediated hypofibrinolysis and hyperfibrinolysis are summarized, with the view of proposing an innovative view of epithelial ion transport in preventing the dysfunction of fibrinolytic system during the progress of COVID-19.
Identifiants
pubmed: 37172333
pii: S0753-3322(23)00653-4
doi: 10.1016/j.biopha.2023.114863
pmc: PMC10169260
pii:
doi:
Substances chimiques
spike protein, SARS-CoV-2
0
Spike Glycoprotein, Coronavirus
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
114863Informations de copyright
Copyright © 2023 The Authors. Published by Elsevier Masson SAS.. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of Competing Interest The authors declare no competing interests.
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