TGF-β signaling and the development of osteoarthritis

Abstract

Osteoarthritis (OA) is a common joint degenerative disease affecting the whole joint structure, including articular cartilage, subchondral bone and synovial tissue. Although extensive work has been done in recent years to explore the molecular mechanism underlying this disease, the pathogenesis of OA is still poorly understood and currently, there is no effective disease-modifying treatment for OA. Recently, both in vitro and in vivo studies suggest that confirmed (TGF-β)/SMAD pathway plays a critical role during OA development. This short review will focus on the function and signaling mechanisms of TGF-β/SMAD pathway in articular chondrocytes, mesenchymal progenitor cells of subchondral bone and synovial lining cells during OA development.

Osteoarthritis: Pathway to therapy

A regulatory pathway that plays a role in the development of osteoarthritis should be a priority target for treatment, say researchers. Osteoarthritis (OA) causes pain and reduced mobility in millions of people worldwide but the mechanisms that trigger and accelerate the disease are poorly understood. Di Chen and co-workers at the University of Rochester and Rush University in the US, reviewed recent papers that link the regulatory pathway of the protein TGF-β (transforming growth factor β) to the development of OA. They confirmed that TGF-β increases the volume of cells in cartilage, promotes the differentiation of cells that can synthesize bone and strengthens linings within joints. The researchers identify genes related to TGF-β that could serve as targets for OA therapy, and urge further research into three other regulatory pathways that interact with TGF-β.

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