Chondrogenic overexpression of miR-146a or intra-articular administration of a Notch1 inhibitor alleviates IL-1β-induced catabolism and rescues joint degeneration in miR-146a-deficient mice, suggesting that miR-146a is sufficient to protect OA pathogenesis by inhibiting Notch signaling in the joint.
The IL-1 ligand cluster encodes for susceptibility to knee OA but not to hip OA, highlighting the genetic heterogeneity of this common, complex disease.