Ruocco Maria Grazia, Karin Michael
Laboratory of Gene Regulation and Signal Transduction, School of Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093, USA.
Adv Exp Med Biol. 2007;602:125-34. doi: 10.1007/978-0-387-72009-8_16.
Transcription factor NF-kappaB has been well recognized as a pivotal player in osteclastogenesis and inflammation-induced bone loss. Here, we discuss our recent results obtained using a genetic approach in mice that indicate the importance of IKKbeta, and not IKKalpha, as a transducer of signals from receptor activator of NF-kappaB (RANK) to NF-kappaB. Ablation of IKKbeta results in lack of osteoclastogenesis and unresponsiveness of IKKbeta-deficient mice to inflammation-induced bone loss. In the need of a more effective therapy for the treatment of inflammatory diseases causing bone resorption, specific inhibition of IKKbeta represents a logical alternative strategy to the current therapies.
转录因子核因子-κB（NF-κB）已被公认为破骨细胞生成和炎症诱导性骨质流失中的关键因子。在此，我们讨论了我们最近利用基因方法在小鼠中获得的结果，这些结果表明IKKβ而非IKKα作为核因子-κB受体激活剂（RANK）信号向NF-κB转导的介质的重要性。IKKβ的缺失导致破骨细胞生成缺乏，且IKKβ缺陷小鼠对炎症诱导性骨质流失无反应。鉴于需要一种更有效的疗法来治疗导致骨吸收的炎症性疾病，特异性抑制IKKβ是当前疗法的一种合理替代策略。
Zotero 插件