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To this end, Chen et al., has suggested that activation of GLP-1R with liraglutide could protect chondrocytes against endoplasmic reticulum (ER) stress, apoptosis and inflammation by decreasing the release of inflammatory mediators and regulating phosphoinositide 3-kinase (PI3K)/AKT signaling, which suggests that GLP-1R is a therapeutic target for the treatment of OA and that liraglutide could be a therapeutic candidate for clinical application [10]

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This tends to be dose-dependent