What is it about?
Inflammation is often linked to increased acidity in tissues, which can activate specific receptors such as GPR65. In this study, we found that activation of GPR65 in cells lining the knee joints of mice and humans triggers the release of molecules that attract immune cells, leading to inflammation as well as increased pain sensitivity.
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Photo by Towfiqu barbhuiya on Unsplash
Why is it important?
Current pain-relief drugs for inflammatory conditions, like arthritis often don't work well enough and can have serious side effects. To develop better treatments, it’s important to identify the key players that cause pain during inflammation. Our findings suggest that blocking the receptor GPR65 could be a promising way to reduce pain for people living with inflammatory conditions.
Perspectives
Chronic pain greatly impacts quality of life. I hope this research inspires further studies on acid-sensitive receptors, like GPR65, as potential drug targets, paving the way for safer and more effective pain treatments to reach patients sooner.
Luke Pattison
University of Cambridge
Inflammatory pain is complex and different mechanisms will likely predominate in different individuals with the same condition. This work highlights the role of the GPR65 receptor in mediating cell-cell interactions to generate pain, thus providing further information about a signalling mechanism that could lead to novel therapeutic approaches.
Ewan Smith
Read the Original
This page is a summary of: Activation of the proton-sensing GPCR, GPR65 on fibroblast-like synoviocytes contributes to inflammatory joint pain, Proceedings of the National Academy of Sciences, December 2024, Proceedings of the National Academy of Sciences,
DOI: 10.1073/pnas.2410653121.
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