Nuclear factor-kappaB (NF-κB) proteins constitute a family of transcription factors that are stimulated by pro-inflammatory cytokines, chemokines, stress-related factors and extracellular matrix (ECM) degradation products. Upon stimulation, the activated NF-κB molecules trigger the expression of an array of genes which induce destruction of the articular joint, leading to osteoarthritis (OA) onset and progression. Therefore, targeted strategies that interfere with NF-κB signalling could offer novel potential therapeutic options for OA treatment. In this review, we discuss the involvement of NF-κB in OA pathogenesis and how pharmacological inhibition of the NF-κB signalling pathway affects OA incidence and evolution.
Keywords: Cartilage destruction; Chondrocytes; NF-κB; Osteoarthritis; Signal transduction.
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