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Developments in these areas aim not only to reduce symptoms, as current treatment options do, but also to restore thyroid function
The proton-activated GPR4 regulates OA pathogenesis via modulating CXCL12/CXCR7 signaling, and inhibition of GPR4 with NE52-QQ57 ameliorates OA development in both mouse models and human articular cartilage explants (169)
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