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NLRP3炎性小体在激素性股骨头坏死骨代谢及其稳态中的作用     被引量:4

Role of NLRP3 inflammasome in the bone metabolism and homeostasis of steroid-induced femoral head necrosis

文献类型:期刊文献

中文题名:NLRP3炎性小体在激素性股骨头坏死骨代谢及其稳态中的作用

英文题名:Role of NLRP3 inflammasome in the bone metabolism and homeostasis of steroid-induced femoral head necrosis

作者:胡康一[1];曹林忠[1,2];万超超[1];尚征亚[1];杨小瑞[1];张勇杰[1]

第一作者:胡康一

机构:[1]甘肃中医药大学,甘肃兰州730000;[2]甘肃中医药大学附属医院,甘肃兰州730000

第一机构:甘肃中医药大学

年份:2023

卷号:29

期号:5

起止页码:701

中文期刊名:中国骨质疏松杂志

外文期刊名:Chinese Journal of Osteoporosis

收录:CSTPCD;;北大核心:【北大核心2020】;CSCD:【CSCD2023_2024】;

基金:国家自然科学基金项目(81860859,82160915)。

语种:中文

中文关键词:NLRP3炎性小体;激素性股骨头坏死;成骨细胞;破骨细胞;骨髓间充质干细胞

外文关键词:NLRP3 inflammasome;steroid-induced femoral head necrosis;osteoblasts;osteoclasts;bone marrow mesenchymal stem cells

摘要:大量的糖皮质激素使用导致股骨头中骨代谢及稳态失衡是激素性股骨头坏死的重要机制之一。细胞焦亡关键因子NLRP3炎性小体在SANFH机制中发挥着重要作用,明确NLRP3炎性小体的结构,激活途径和调控机制,以及NLRP3炎性小体和下游炎性因子IL-1β、IL-18对激素性股骨头坏死中成骨细胞、破骨细胞以及骨髓间充质干细胞的作用机制,将为激素性股骨头坏死的防治提供新的思路与靶点。该文对NLRP3炎性小体在骨代谢及稳态中的相关作用机制进行综述,系统阐述NLRP3炎性小体与SANFH成骨和破骨分化中的具体作用机制,以期为临床治疗和基础研究提供一定的借鉴。
The imbalance of bone metabolism and homeostasis in the femoral head caused by excessive use of glucocorticoids is one of the important mechanisms of hormone-induced femoral head necrosis.NLRP3 inflammasome,a key cytokine of pyrodeath,plays an important role in the SANFH mechanism.To clarify the structure,activation pathway and regulatory mechanism of the NLRP3 inflammasome,and the mechanism of NLRP3 inflammasome and downstream inflammatory factors IL-1βand IL-18 on osteoblasts,osteoclasts,and bone marrow mesenchymal stem cells in steroid-induced femoral head necrosis,may provide new ideas and targets for the prevention and treatment of steroid-induced femoral head necrosis.In this paper,the relevant mechanism of NLRP3 inflammasome in bone metabolism and homeostasis is reviewed.The specific mechanism of NLRP3 inflammasome in SANFH osteogenesis and osteoclast differentiation are systematically expounded.This may provide some references for clinical treatment and basic research.

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