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2020 ; 144
(ä): 110012
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Targeting adenosinergic pathway and adenosine A(2A) receptor signaling for the
treatment of COVID-19: A hypothesis
#MMPMID32590324
Abouelkhair MA
Med Hypotheses
2020[Nov]; 144
(ä): 110012
PMID32590324
show ga
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.
|*COVID-19 Drug Treatment
[MESH]
|*Pandemics
[MESH]
|5'-Nucleotidase/metabolism
[MESH]
|Adaptive Immunity/drug effects
[MESH]
|Adenosine A2 Receptor Antagonists/pharmacology/*therapeutic use
[MESH]