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破骨细胞生成及骨疾病中的RANKL-RANK信号传导

RANKL-RANK signaling in osteoclastogenesis and bone disease.

作者信息

Wada Teiji, Nakashima Tomoki, Hiroshi Nishina, Penninger Josef M

机构信息

Institute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA), Dr. Bohrgasse 3, A-1030 Vienna, Austria.

出版信息

Trends Mol Med. 2006 Jan;12(1):17-25. doi: 10.1016/j.molmed.2005.11.007. Epub 2005 Dec 13.

Abstract

Hundreds of millions of people worldwide are affected by bone-related diseases, such as osteoporosis and rheumatoid arthritis. Understanding the molecular mechanisms of bone metabolism is crucial for developing novel drugs for treating such diseases. In particular, genetic experiments showing that the receptor activator of NF-kappaB (RANK), its ligand RANKL, and the decoy receptor OPG are essential, central regulators of osteoclast development and osteoclast function were significant turning points in our understanding of bone diseases. RANKL-RANK signaling activates a variety of downstream signaling pathways required for osteoclast development. Moreover, molecular cross-talk between RANKL-RANK and other ligand-receptor systems fine-tunes bone homeostasis in normal physiology and disease. Designing novel drugs that target RANKL-RANK and their signaling pathways in osteoclasts could potentially revolutionize the treatment of many diseases associated with bone loss such as arthritis, tooth loss, cancer metastases or osteoporosis.

摘要

全球数亿人受到与骨骼相关的疾病影响,如骨质疏松症和类风湿性关节炎。了解骨代谢的分子机制对于开发治疗此类疾病的新型药物至关重要。特别是,基因实验表明核因子κB受体激活剂(RANK)、其配体RANKL和诱饵受体骨保护素(OPG)是破骨细胞发育和破骨细胞功能的重要核心调节因子,这是我们对骨疾病理解的重大转折点。RANKL-RANK信号激活破骨细胞发育所需的多种下游信号通路。此外,RANKL-RANK与其他配体-受体系统之间的分子相互作用在正常生理和疾病状态下微调骨稳态。设计靶向破骨细胞中RANKL-RANK及其信号通路的新型药物可能会彻底改变许多与骨质流失相关疾病的治疗方式,如关节炎、牙齿脱落、癌症转移或骨质疏松症。

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