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. 2016 May 4;76(1):218–226. doi: 10.1136/annrheumdis-2015-208577

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Cartilage injury causes activation of WNT signalling through downregulation of antagonists such as FRZB and upregulation of several agonists such as WNT16 and WNT8.¹⁴ ¹⁸ WNT16 buffers the canonical WNT activation to homeostatic levels through its capacity to directly support a weak activation and preventing excessive activation induced by other ligands. Excessive canonical WNT activation causes cartilage breakdown by driving inappropriate maturation particularly within the superficial zone progenitor cells,⁸ ¹⁸ whereas homeostatic levels of activation are necessary for supporting the superficial progenitor population and lubricin expression (this work and refs ⁵^,⁷).