Molecular signaling pathways, pathophysiological features in various organs, and treatment strategies in SARS-CoV2 infection.
ACE2
COVID-19
SARS-CoV-2
Signaling pathways
Journal
Acta histochemica
ISSN: 1618-0372
Titre abrégé: Acta Histochem
Pays: Germany
ID NLM: 0370320
Informations de publication
Date de publication:
Jul 2022
Jul 2022
Historique:
received:
04
05
2022
accepted:
19
05
2022
pubmed:
7
6
2022
medline:
18
6
2022
entrez:
6
6
2022
Statut:
ppublish
Résumé
Cytokine storms and extra-activated cytokine signaling pathways can lead to severe tissue damage and patient death. Activation of inflammatory signaling pathways during Cytokine storms are an important factor in the development of acute respiratory syndrome (SARS-CoV-2), which is the major health problem today, causing systemic and local inflammation. Cytokine storms attract many inflammatory cells that attack the lungs and other organs and cause tissue damage. Angiotensin-converting enzyme 2 (ACE2) are expressed in a different type of tissues. inhibition of ACE2 activity impairs renin-angiotensin (RAS) function, which is related to the severity of symptoms and mortality rate in COVID-19 patients. Different signaling cascades are activated, affecting various organs during SARS-CoV-2 infection. Nowadays, there is no specific treatment for COVID-19, but scientists have recognized and proposed several treatment alternatives, including applying cytokine inhibitors, immunomodulators, and plasma therapy. Herein, we have provided the detailed mechanism of SARS-CoV-2 induced cytokine signaling and its connection with pathophysiological features in different organs. Possible treatment options to cope with the severe clinical manifestations of COVID-19 are also discussed.
Identifiants
pubmed: 35662001
pii: S0065-1281(22)00067-8
doi: 10.1016/j.acthis.2022.151908
pmc: PMC9130726
pii:
doi:
Substances chimiques
Cytokines
0
Angiotensin-Converting Enzyme 2
EC 3.4.17.23
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
151908Informations de copyright
Copyright © 2022 Elsevier GmbH. All rights reserved.
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