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Tytuł pozycji:

Targeting adenosinergic pathway and adenosine A 2A receptor signaling for the treatment of COVID-19: A hypothesis.

Tytuł:
Targeting adenosinergic pathway and adenosine A 2A receptor signaling for the treatment of COVID-19: A hypothesis.
Autorzy:
Abouelkhair MA; Department of Biomedical and Diagnostic Sciences, University of Tennessee College of Veterinary Medicine, 2407 River Dr, Knoxville, TN 37996, USA. Electronic address: .
Źródło:
Medical hypotheses [Med Hypotheses] 2020 Nov; Vol. 144, pp. 110012. Date of Electronic Publication: 2020 Jun 19.
Typ publikacji:
Journal Article
Język:
English
Imprint Name(s):
Publication: New York : Elsevier, 2002- : Eden Press
Original Publication: Penrith, Eng., Eden Press.
MeSH Terms:
Pandemics*
COVID-19 Drug Treatment*
Adenosine A2 Receptor Antagonists/*therapeutic use
Receptor, Adenosine A2A/*physiology
5'-Nucleotidase/metabolism ; Adaptive Immunity/drug effects ; Adenosine A2 Receptor Antagonists/pharmacology ; Adenosine Triphosphate/metabolism ; Apyrase/metabolism ; COVID-19/epidemiology ; COVID-19/immunology ; COVID-19/metabolism ; GPI-Linked Proteins/metabolism ; Humans ; Immunity, Innate/drug effects ; Interferon-beta/physiology ; Models, Immunological ; Molecular Targeted Therapy ; Severe acute respiratory syndrome-related coronavirus/immunology ; SARS-CoV-2/immunology ; Signal Transduction/drug effects ; Virus Replication/drug effects
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Contributed Indexing:
Keywords: Adenosine; CD39; CD73; COVID-19; Immunotherapy
Substance Nomenclature:
0 (Adenosine A2 Receptor Antagonists)
0 (GPI-Linked Proteins)
0 (Receptor, Adenosine A2A)
77238-31-4 (Interferon-beta)
8L70Q75FXE (Adenosine Triphosphate)
EC 3.1.3.5 (5'-Nucleotidase)
EC 3.1.3.5 (NT5E protein, human)
EC 3.6.1.5 (Apyrase)
EC 3.6.1.5 (ENTPD1 protein, human)
Entry Date(s):
Date Created: 20200627 Date Completed: 20201204 Latest Revision: 20221207
Update Code:
20240105
PubMed Central ID:
PMC7303042
DOI:
10.1016/j.mehy.2020.110012
PMID:
32590324
Czasopismo naukowe
The most serious health issue today is the rapid outbreak of Coronavirus Disease 2019 (COVID-19). More than 6,973,427 confirmed cases were diagnosed in nearly 213 countries and territories around the world and two international conveyances, causing globally over 400,000 deaths. Epidemiology, risk factors, and clinical characteristics of COVID-19 patients have been identified, but the factors influencing the immune system against COVID-19 have not been well established. Upon infection or cell damage, high amounts of adenosine triphosphate (ATP) are released from damaged cells, which serve as mediators of inflammation through purinergic cell surface receptor signaling. As a protective mechanism to prevent excessive damage to host tissue, adenosine counteracts ATP's effects by adenosine receptor stimulation to suppress the pro-inflammatory response. Adenosine is seen as a major obstacle to the efficacy of immune therapies, and the adenosinergic axis components are critical therapeutic targets for cancer and microbial infections. Pharmacologic inhibitors or antibodies specific to adenosinergic pathway components or adenosine receptors in microbial and tumor therapy have shown efficacy in pre-clinical studies and are entering the clinical arena. In this review, we provide a novel hypothesis explaining the potential for improving the efficiency of innate and adaptive immune systems by targeting adenosinergic pathway components and adenosine A 2A receptor signaling for the treatment of COVID-19.
(Copyright © 2020 Elsevier Ltd. All rights reserved.)

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