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 …