Purinergic signaling in the modulation of redox biology.


Journal

Redox biology
ISSN: 2213-2317
Titre abrégé: Redox Biol
Pays: Netherlands
ID NLM: 101605639

Informations de publication

Date de publication:
11 2021
Historique:
received: 09 09 2021
accepted: 14 09 2021
pubmed: 27 9 2021
medline: 1 12 2021
entrez: 26 9 2021
Statut: ppublish

Résumé

Purinergic signaling is a cell communication pathway mediated by extracellular nucleotides and nucleosides. Tri- and diphosphonucleotides are released in physiological and pathological circumstances activating purinergic type 2 receptors (P2 receptors): P2X ion channels and P2Y G protein-coupled receptors. The activation of these receptors triggers the production of reactive oxygen and nitrogen species and alters antioxidant defenses, modulating the redox biology of cells. The activation of P2 receptors is controlled by ecto-enzymes named ectonucleotidases, E-NTPDase1/CD39 and ecto-5'-nucleotidase/CD73) being the most relevant. The first enzyme hydrolyzes adenosine triphosphate (ATP) and adenosine diphosphate (ADP) into adenosine monophosphate (AMP), and the second catalyzes the hydrolysis of AMP to adenosine. The activity of these enzymes is diminished by oxidative stress. Adenosine actives P1 G-coupled receptors that, in general, promote the maintenance of redox hemostasis by decreasing reactive oxygen species (ROS) production and increase antioxidant enzymes. Intracellular purine metabolism can also contribute to ROS generation via xanthine oxidase activity, which converts hypoxanthine into xanthine, and finally, uric acid. In this review, we describe the mechanisms of redox biology modulated by purinergic signaling and how this signaling may be affected by disturbances in the redox homeostasis of cells.

Identifiants

pubmed: 34563872
pii: S2213-2317(21)00296-2
doi: 10.1016/j.redox.2021.102137
pmc: PMC8479832
pii:
doi:

Substances chimiques

Adenosine Diphosphate 61D2G4IYVH
Adenosine Triphosphate 8L70Q75FXE
Adenosine K72T3FS567

Types de publication

Journal Article Research Support, Non-U.S. Gov't Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

102137

Informations de copyright

Copyright © 2021. Published by Elsevier B.V.

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Auteurs

Luiz Eduardo Baggio Savio (LEB)

Instituto de Biofísica Carlos Chagas Filho, Universidade Federal Do Rio de Janeiro, Rio de Janeiro, Brazil. Electronic address: savio@biof.ufrj.br.

Raíssa Leite-Aguiar (R)

Instituto de Biofísica Carlos Chagas Filho, Universidade Federal Do Rio de Janeiro, Rio de Janeiro, Brazil.

Vinícius Santos Alves (VS)

Instituto de Biofísica Carlos Chagas Filho, Universidade Federal Do Rio de Janeiro, Rio de Janeiro, Brazil.

Robson Coutinho-Silva (R)

Instituto de Biofísica Carlos Chagas Filho, Universidade Federal Do Rio de Janeiro, Rio de Janeiro, Brazil.

Angela T S Wyse (ATS)

Laboratório de Neuroproteção e Doenças Metabólicas, Departamento de Bioquímica, ICBS, Universidade Federal Do Rio Grande Do Sul, Porto Alegre, RS, Brazil.

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