Noggin, an inhibitor of bone morphogenetic protein signaling, antagonizes TGF-β1 in a mouse model of osteoarthritis.

Abstract Osteoarthritis (OA) is the most common joint disease worldwide; however, disease-modifying treatments are lacking because of the complicated pathological mechanisms. As a breakthrough, aberrant activation of transforming growth factor-β 1 (TGF-β1)in subchondral bone has been confirmed as an essential pathomechanism for OA progression, and has become a potential therapeutic target. In addition to RD thus, it seems promising for OA treatment.