Possible Role of Adenosine in COVID-19 Pathogenesis and Therapeutic Opportunities.

COVID acute lung injury adenosine adenosine deaminase adenosine kinase coronavirus

Journal

Frontiers in pharmacology
ISSN: 1663-9812
Titre abrégé: Front Pharmacol
Pays: Switzerland
ID NLM: 101548923

Informations de publication

Date de publication:
2020
Historique:
received: 13 08 2020
accepted: 21 10 2020
entrez: 16 12 2020
pubmed: 17 12 2020
medline: 17 12 2020
Statut: epublish

Résumé

The outbreak of the novel coronavirus disease 2019 (COVID-19) caused by Severe Acute Respiratory Syndrome CoronaVirus-2 (SARS-CoV-2) requires urgent clinical interventions. Crucial clinical needs are: 1) prevention of infection and spread of the virus within lung epithelia and between people, 2) attenuation of excessive lung injury in Advanced Respiratory Distress Syndrome, which develops during the end stage of the disease, and 3) prevention of thrombosis associated with SARS-CoV-2 infection. Adenosine and the key adenosine regulators adenosine deaminase (ADA), adenosine kinase (ADK), and equilibrative nucleoside transporter 1 may play a role in COVID-19 pathogenesis. Here, we highlight 1) the non-enzymatic role of ADA by which it might out-compete the virus (SARS-CoV-2) for binding to the CD26 receptor, 2) the enzymatic roles of ADK and ADA to increase adenosine levels and ameliorate Advanced Respiratory Distress Syndrome, and 3) inhibition of adenosine transporters to reduce platelet activation, thrombosis and improve COVID-19 outcomes. Depending on the stage of exposure to and infection by SARS-CoV-2, enhancing adenosine levels by targeting key adenosine regulators such as ADA, ADK and equilibrative nucleoside transporter 1 might find therapeutic use against COVID-19 and warrants further investigation.

Identifiants

pubmed: 33324223
doi: 10.3389/fphar.2020.594487
pii: 594487
pmc: PMC7726428
doi:

Types de publication

Journal Article

Langues

eng

Pagination

594487

Subventions

Organisme : NINDS NIH HHS
ID : R01 NS103740
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS065957
Pays : United States
Organisme : NIGMS NIH HHS
ID : U54 GM115458
Pays : United States
Organisme : NIMH NIH HHS
ID : R01 MH119000
Pays : United States
Organisme : NIMH NIH HHS
ID : R01 MH100972
Pays : United States
Organisme : NIMH NIH HHS
ID : R01 MH105329
Pays : United States
Organisme : NIDA NIH HHS
ID : R01 DA032444
Pays : United States

Informations de copyright

Copyright © 2020 Geiger, Khan, Murugan and Boison.

Déclaration de conflit d'intérêts

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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Auteurs

Jonathan D Geiger (JD)

Department of Biomedical Sciences, University of North Dakota School of Medicine and Health Sciences, Grand Forks, ND, United States.

Nabab Khan (N)

Department of Biomedical Sciences, University of North Dakota School of Medicine and Health Sciences, Grand Forks, ND, United States.

Madhuvika Murugan (M)

Department of Neurosurgery, Robert Wood Johnson Medical School, Rutgers University, Piscataway, NJ, United States.

Detlev Boison (D)

Department of Neurosurgery, Robert Wood Johnson Medical School, Rutgers University, Piscataway, NJ, United States.
Rutgers Neurosurgery H.O.P.E. Center, Department of Neurosurgery, Rutgers University, New Brunswick, NJ, United States.

Classifications MeSH