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

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

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.