转化生长因子β1/Smad信号通路在破骨细胞分化发育中的研究进展  

Transforming growth factorβ1/Smad signaling pathway in osteoclast differentiation and development:research progress

作　　者：庄新晨 苏佳灿[1] ZHUANG Xin-chen;SU Jia-can(Department of Trauma Orthopaedics,The First Affiliated Hospital of Naval Medical University(Second Military Medical University),Shanghai 200433,China)

机构地区：[1]海军军医大学(第二军医大学)第一附属医院创伤骨科,上海200433

出　　处：《海军军医大学学报》2023年第5期622-626,共5页Academic Journal of Naval Medical University

基　　金：国家自然科学基金(82172098)。

摘　　要：破骨细胞是来源于单核造血髓系细胞的多核巨细胞,它的激活在炎症性骨破坏及骨质疏松症的发生和发展中起着十分重要的作用。破骨细胞的分化和功能受到多种细胞因子和生长因子的调节,已有研究表明,TGF-β1与其下游信号转导蛋白Smad2/3、Smad1/5可促进或抑制破骨细胞分化、发育和成熟,其机制与调节核因子κB受体激活蛋白配体(RANKL)/核因子κB受体激活蛋白(RANK)信号通路及其下游介质有关。本文主要针对TGF-β1/Smad信号通路在破骨细胞分化和发育中的作用进行综述。Osteoclasts are multinucleated macrophages derived from mononuclear hematopoietic myeloid cells,and their activation plays a very important role in the development and progression of inflammatory bone destruction and osteoporosis.The differentiation and function of osteoclasts are regulated by a variety of cytokines and growth factors.Previous studies have shown that transforming growth factorβ1(TGF-β1)and its downstream signal transduction proteins Smad2/3 and Smad1/5 can promote or inhibit the differentiation,development and maturation of osteoclasts,and its mechanism is related to regulating the receptor activator of nuclear factorκB ligand(RANKL)/receptor activator of nuclear factorκB factor(RANK)signaling pathway and its downstream mediators.This paper mainly reviews the roles of TGF-β1/Smad signaling pathway in the differentiation and development of osteoclasts.

关 键 词：破骨细胞 转化生长因子Β SMAD蛋白 核因子κB受体激活蛋白配体 

分 类 号：R336[医药卫生—人体生理学]