Adenosine Metabolized From Extracellular Atp Ameliorates Organ Injury By Triggering A2Br Signaling

Authors

Taha Kelestemur
Zoltán H Németh
Pal Pacher
Jennet Beesley
Simon C Robson
Holger K Eltzschig
György Haskó

Language

English

Publication Date

7-13-2023

Journal

Respiratory Research

DOI

10.1186/s12931-023-02486-3

PMID

37438813

PMCID

PMC10339538

PubMedCentral® Posted Date

July 2023

PubMedCentral® Full Text Version

Post-print

Abstract

BACKGROUND: Trauma and a subsequent hemorrhagic shock (T/HS) result in insufficient oxygen delivery to tissues and multiple organ failure. Extracellular adenosine, which is a product of the extracellular degradation of adenosine 5' triphosphate (ATP) by the membrane-embedded enzymes CD39 and CD73, is organ protective, as it participates in signaling pathways, which promote cell survival and suppress inflammation through adenosine receptors including the A

METHODS: T/HS shock was induced by blood withdrawal from the femoral artery in wild-type, global knockout (CD39, CD73, A

RESULTS: T/HS upregulated the expression of CD39, CD73, and the A

CONCLUSION: In conclusion, the CD39-CD73-A

Keywords

A2BR, Acute lung injury, Adenosine, CD39, CD73, Trauma hemorrhagic shock

Published Open-Access

yes

Recommended Citation

Kelestemur, Taha; Németh, Zoltán H; Pacher, Pal; et al., "Adenosine Metabolized From Extracellular Atp Ameliorates Organ Injury By Triggering A2Br Signaling" (2023). Faculty, Staff and Student Publications. 784.
https://digitalcommons.library.tmc.edu/uthmed_docs/784