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The Wnt inhibitor Tiki2 maintains articular cartilage homeostasis and protects against osteoarthritis
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DOI：10.1126/scisignal.adv0789.png)
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Abstract
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Excessive Wnt signaling in articular chondrocytes leads to cartilage degeneration and is associated with osteoarthritis (OA). Li et al. investigated the role of the Wnt-cleaving cell surface protease Tiki2 in the articular cartilage in male mice and in primary mouse and human chondrocytes. Tiki2 was required for maintenance of knee cartilage, promoted chondrocyte differentiation, and attenuated both β-catenin–dependent and β-catenin–independent signaling in chondrocytes. Chondrocyte-specific loss of Tiki2 exacerbated OA caused by surgical destabilization of the knee, whereas localized overexpression of human TIKI2 in the joint protected against OA-associated cartilage loss. The findings suggest augmenting TIKI2 activity as a potential Wnt-limiting strategy for therapeutic intervention in OA. —Annalisa M. VanHook
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