Targeting adenosine receptors might be a promising approach to promote bone regeneration, according to new research. The platelet aggregation inhibitor ticagrelor, which also blocks cellular uptake of adenosine, inhibited osteoclast differentiation in vitro, an effect that was abrogated by inhibition of the A2A adenosine receptor. Moreover, ticagrelor and clopidogrel (another antiplatelet agent) promoted bone regeneration in mice with calvarial defects as effectively as BMP2, a growth factor currently marketed to promote bone growth and regeneration.
References
Mediero, A. et al. Ticagrelor regulates osteoblast and osteoclast function and promotes bone formation in vivo via an adenosine-dependent mechanism. FASEB J. http://dx.doi.org/10.1096/fj.201600616R (2016)
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Holmes, D. Antiplatelet agent promotes bone formation. Nat Rev Endocrinol 12, 626 (2016). https://doi.org/10.1038/nrendo.2016.145
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DOI: https://doi.org/10.1038/nrendo.2016.145