Does Adenosine Triphosphate via Purinergic Receptor Signalling Fuel Pulmonary Fibrosis?

Background: Interstitial lung diseases (ILD) are poorly understood disorders characterised by diffuse damage to the lung parenchyma, with inflammation and fibrosis. Some manifest a progressive fibrotic phenotype with high fatality and limited treatment options, such as idiopathic pulmonar...

Full description

Saved in:
Bibliographic Details
Main Authors: Luke Forde, Debananda Gogoi, Rory Baird, Cormac McCarthy, Michael P. Keane, Emer P. Reeves, Emmet E. McGrath
Format: Article
Language:English
Published: Karger Publishers 2025-01-01
Series:Journal of Innate Immunity
Online Access:https://karger.com/article/doi/10.1159/000543083
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1849321731633709056
author Luke Forde
Debananda Gogoi
Rory Baird
Cormac McCarthy
Michael P. Keane
Emer P. Reeves
Emmet E. McGrath
author_facet Luke Forde
Debananda Gogoi
Rory Baird
Cormac McCarthy
Michael P. Keane
Emer P. Reeves
Emmet E. McGrath
author_sort Luke Forde
collection DOAJ
description Background: Interstitial lung diseases (ILD) are poorly understood disorders characterised by diffuse damage to the lung parenchyma, with inflammation and fibrosis. Some manifest a progressive fibrotic phenotype with high fatality and limited treatment options, such as idiopathic pulmonary fibrosis. Summary: The degree to which inflammation plays a role in fibrosis progression is unknown. However, wound healing and fibrosis are intricate processes influenced by various inflammatory factors. Extracellular nucleosides and nucleotides, including adenosine triphosphate, activate pro-inflammatory responses to innate immunity and are widely implicated in tissue fibrosis across different organs. The pro-inflammatory effects of extracellular nucleotides occur via P1 and P2 purinergic receptors, expressed across the lung and immune system, and have been implicated in various pulmonary diseases including pulmonary fibrosis. This review amalgamates available data on the complex role of P1 and P2 purinergic receptor signalling in pulmonary fibrosis and discusses perspectives for novel treatments. Key Messages: Purinergic signalling plays a complex and pivotal role in pulmonary fibrosis, warranting further study. The intricate interplay between P1 and P2 receptor pathways necessitates a comprehensive approach to understand their collective impact. While evidence from preclinical models is promising, human studies are essential for further understanding of pulmonary fibrosis. Advances in receptor-specific agonists and antagonists provide novel avenues for research and may ultimately lead to new therapies for patients.
format Article
id doaj-art-8a99339d9ea24507a777ec14b6ecb1f2
institution Kabale University
issn 1662-8128
language English
publishDate 2025-01-01
publisher Karger Publishers
record_format Article
series Journal of Innate Immunity
spelling doaj-art-8a99339d9ea24507a777ec14b6ecb1f22025-08-20T03:49:41ZengKarger PublishersJournal of Innate Immunity1662-81282025-01-01171445510.1159/000543083Does Adenosine Triphosphate via Purinergic Receptor Signalling Fuel Pulmonary Fibrosis?Luke Fordehttps://orcid.org/0000-0002-3738-6512Debananda Gogoihttps://orcid.org/0000-0003-3108-8001Rory BairdCormac McCarthyMichael P. KeaneEmer P. Reeveshttps://orcid.org/0000-0002-1922-0447Emmet E. McGrath Background: Interstitial lung diseases (ILD) are poorly understood disorders characterised by diffuse damage to the lung parenchyma, with inflammation and fibrosis. Some manifest a progressive fibrotic phenotype with high fatality and limited treatment options, such as idiopathic pulmonary fibrosis. Summary: The degree to which inflammation plays a role in fibrosis progression is unknown. However, wound healing and fibrosis are intricate processes influenced by various inflammatory factors. Extracellular nucleosides and nucleotides, including adenosine triphosphate, activate pro-inflammatory responses to innate immunity and are widely implicated in tissue fibrosis across different organs. The pro-inflammatory effects of extracellular nucleotides occur via P1 and P2 purinergic receptors, expressed across the lung and immune system, and have been implicated in various pulmonary diseases including pulmonary fibrosis. This review amalgamates available data on the complex role of P1 and P2 purinergic receptor signalling in pulmonary fibrosis and discusses perspectives for novel treatments. Key Messages: Purinergic signalling plays a complex and pivotal role in pulmonary fibrosis, warranting further study. The intricate interplay between P1 and P2 receptor pathways necessitates a comprehensive approach to understand their collective impact. While evidence from preclinical models is promising, human studies are essential for further understanding of pulmonary fibrosis. Advances in receptor-specific agonists and antagonists provide novel avenues for research and may ultimately lead to new therapies for patients.https://karger.com/article/doi/10.1159/000543083
spellingShingle Luke Forde
Debananda Gogoi
Rory Baird
Cormac McCarthy
Michael P. Keane
Emer P. Reeves
Emmet E. McGrath
Does Adenosine Triphosphate via Purinergic Receptor Signalling Fuel Pulmonary Fibrosis?
Journal of Innate Immunity
title Does Adenosine Triphosphate via Purinergic Receptor Signalling Fuel Pulmonary Fibrosis?
title_full Does Adenosine Triphosphate via Purinergic Receptor Signalling Fuel Pulmonary Fibrosis?
title_fullStr Does Adenosine Triphosphate via Purinergic Receptor Signalling Fuel Pulmonary Fibrosis?
title_full_unstemmed Does Adenosine Triphosphate via Purinergic Receptor Signalling Fuel Pulmonary Fibrosis?
title_short Does Adenosine Triphosphate via Purinergic Receptor Signalling Fuel Pulmonary Fibrosis?
title_sort does adenosine triphosphate via purinergic receptor signalling fuel pulmonary fibrosis
url https://karger.com/article/doi/10.1159/000543083
work_keys_str_mv AT lukeforde doesadenosinetriphosphateviapurinergicreceptorsignallingfuelpulmonaryfibrosis
AT debanandagogoi doesadenosinetriphosphateviapurinergicreceptorsignallingfuelpulmonaryfibrosis
AT rorybaird doesadenosinetriphosphateviapurinergicreceptorsignallingfuelpulmonaryfibrosis
AT cormacmccarthy doesadenosinetriphosphateviapurinergicreceptorsignallingfuelpulmonaryfibrosis
AT michaelpkeane doesadenosinetriphosphateviapurinergicreceptorsignallingfuelpulmonaryfibrosis
AT emerpreeves doesadenosinetriphosphateviapurinergicreceptorsignallingfuelpulmonaryfibrosis
AT emmetemcgrath doesadenosinetriphosphateviapurinergicreceptorsignallingfuelpulmonaryfibrosis