NLRP3炎性小体参与骨质疏松症关键细胞调节机制的研究进展  

Role of NLRP3 inflammasome in key cellular regulatory mechanisms in osteoporosis

作　　者：李嘉仪 林吉生[1] 费琦[1] LI Jia-yi;LIN Ji-sheng;FEI Qi(Department of Orthopedics,Beijing Friendship Hospital,Capital Medical University,Beijing 100050,China)

机构地区：[1]首都医科大学附属北京友谊医院骨科,北京100050

出　　处：《中华骨质疏松和骨矿盐疾病杂志》2024年第1期62-66,共5页Chinese Journal Of Osteoporosis And Bone Mineral Research

基　　金：北京市自然科学基金(7222033)

摘　　要：近年来的研究表明,慢性炎症和衰老驱动可造成骨量减少,进而导致骨质疏松症的发生,慢性炎症的发生发展又与炎性小体的激活密切相关,其中NLRP3(nucleotide-binding oligomerization domain-like receptor family pyrin domain 3)炎性小体的激活开始引起许多学者的重视。本文通过回顾文献,从NLRP3炎性小体的结构和调控机制,以及NLRP3炎性小体对破骨细胞、成骨细胞和骨髓间充质干细胞的影响,进一步总结NLRP3炎性小体在骨质疏松症发展过程中的作用,为骨质疏松症炎性机制的研究提供新思路。Recent studies have shown that chronic inflammation and aging drive can cause osteopenia,leading to the occurrence of osteoporosis.The occurrence and development of chronic inflammation is closely related to the activation of inflammasomes,among which the activation of nucleotide-binding oligomerization domain-like receptor family pyrin domain 3(NLRP3)inflammasome has attracted the attention.In this article,the literature was reviewed and the structure and regulatory mechanism of NLRP3 inflammasome,the effects of NLRP3 inflammasome on osteoclasts,osteoblasts and bone marrow mesenchymal stem cells,and the role of NLRP3 inflammasome in the development of osteoporosis were summarized,so as to provide new ideas for the study of the inflammatory mechanism of osteoporosis.

关 键 词：NLRP3 骨质疏松症 炎性小体 成骨细胞 破骨细胞 

分 类 号：R589.5[医药卫生—内分泌]