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Does Adenosine Triphosphate via Purinergic Receptor Signalling Fuel Pulmonary Fibrosis?
Luke Forde1,2, Debananda Gogoi3, Rory Baird3
1Pulmonary Clinical Science, Department of Anaesthesia and Critical Care Medicine, Royal College of Surgeons in Ireland, University of Medicine and Health Sciences, Dublin, Ireland, lukeforde23@rcsi.ie.
Inflammation and fibrosis in interstitial lung diseases (ILD) are complex. Extracellular nucleotides acting via P1 and P2 purinergic receptors significantly influence pulmonary fibrosis, suggesting novel therapeutic targets.
Area of Science:
- Pulmonary Medicine
- Immunology
- Cell Biology
Background:
- Interstitial lung diseases (ILD) involve diffuse lung damage, inflammation, and fibrosis.
- Progressive fibrotic ILDs, like idiopathic pulmonary fibrosis, have high fatality and limited treatments.
Purpose of the Study:
- To review the role of P1 and P2 purinergic receptor signaling in pulmonary fibrosis.
- To discuss potential novel therapeutic strategies targeting purinergic pathways.
Main Methods:
- Literature review of existing data on purinergic signaling in pulmonary fibrosis.
- Analysis of the interplay between inflammation, extracellular nucleotides, and fibrosis progression.
Main Results:
- Extracellular nucleotides activate pro-inflammatory responses via P1 and P2 purinergic receptors.
- These receptors are implicated in tissue fibrosis across organs, including the lungs.
- Purinergic signaling is a key factor in pulmonary fibrosis development and progression.
Conclusions:
- Purinergic signaling plays a complex and pivotal role in pulmonary fibrosis.
- Further research, including human studies, is essential to understand these pathways.
- Targeting P1 and P2 receptors offers potential for new pulmonary fibrosis therapies.
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