NF-κB
骨关节炎
转录因子
趋化因子
信号转导
癌症研究
刺猬信号通路
αBκ
细胞外基质
细胞生物学
发病机制
促炎细胞因子
炎症
医学
生物
NFKB1型
基因
免疫学
遗传学
病理
替代医学
作者
Stella Rigoglou,Athanasios G. Papavassiliou
标识
DOI:10.1016/j.biocel.2013.08.018
摘要
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.
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