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• W2803755451 abstract "Objective Systemic sclerosis ( SS c; scleroderma) is a chronic disease that affects the skin and various internal organs. Dermal fibrosis is a major component of this disease. The mechanisms that promote dermal fibrosis remain elusive. Elevations in tissue adenosine levels and the subsequent engagement of the profibrotic A 2B adenosine receptor ( ADORA 2B) have been shown to regulate fibrosis in multiple organs including the lung, kidney, and penis; however, the role of ADORA 2B in dermal fibrosis has not been investigated. We undertook this study to test our hypothesis that elevated expression of ADORA 2B in the skin drives the development of dermal fibrosis. Methods We assessed the involvement of ADORA 2B in the regulation of dermal fibrosis using a well‐established mouse model of dermal fibrosis. Using an orally active ADORA 2B antagonist, we demonstrated how inhibition of ADORA 2B results in reduced dermal fibrosis in 2 distinct experimental models. Finally, using human dermal fibroblasts, we characterized the expression of adenosine receptors. Results We demonstrated that levels of ADORA 2B were significantly elevated in dermal fibrosis and that the therapeutic blockade of this receptor in vivo using an ADORA 2B antagonist could reduce the production of profibrotic mediators in the skin and attenuate dermal fibrosis. Antagonism of ADORA 2B resulted in reduced numbers of arginase‐expressing macrophages and myofibroblasts and in reduced levels of the extracellular matrix proteins fibronectin, collagen, and hyaluronan. Conclusion These findings identify ADORA 2B as a potential profibrotic regulator in dermal fibrosis and suggest that ADORA 2B antagonism may be a useful approach for the treatment of SS c." @default.
• W2803755451 created "2018-06-01" @default.
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• W2803755451 date "2018-08-06" @default.
• W2803755451 modified "2023-10-01" @default.
• W2803755451 title "The Antifibrotic Effect of A_2B Adenosine Receptor Antagonism in a Mouse Model of Dermal Fibrosis" @default.
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• W2803755451 doi "https://doi.org/10.1002/art.40554" @default.
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