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.

译文

:核因子-κB(NF-κB)蛋白构成转录因子家族,可被促炎性细胞因子,趋化因子,应激相关因子和细胞外基质(ECM)降解产物刺激。刺激后,活化的NF-κB分子触发一系列基因的表达,这些基因诱导关节的破坏,从而导致骨关节炎(OA)的发作和进展。因此,干扰NF-κB信号传导的靶向策略可以为OA治疗提供新的潜在治疗选择。在这篇综述中,我们讨论了NF-κB在OA发病机理中的参与以及NF-κB信号通路的药理抑制作用如何影响OA的发生和发展。

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