Abstract
Purpose: Osteoarthritis (OA) is a degenerative joint disease characterized by inflammation and irreversible cartilage damage. The development of OA is associated with dysregulated TGF-β signaling. Via intracellular activation of the transcription factors SMAD2 and SMAD3 this growth factor inhibits chondrocyte hypertrophy and expression of cartilage degrading enzymes. Recently, it has been shown that post-translational modification of these SMAD proteins in their linker protein domain can dysregulate TGF-β signaling.
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