自噬在糖皮质激素性骨质疏松症中的作用机制  

Mechanism of autophagy in glucocorticoid-induced osteoporosis

作　　者：张惜燕 胡勇 邢玉瑞[1] ZHANG Xiyan;HU Yong;XING Yurui(Shaanxi University of Chinese Medicine,Xianyang 712046,China)

机构地区：[1]陕西中医药大学,陕西咸阳712046

出　　处：《中国骨质疏松杂志》2022年第6期927-930,共4页Chinese Journal of Osteoporosis

基　　金：陕西省教育厅重点科研计划项目(20JS029,19JS016);陕西中医药大学学科创新团队项目(2019-YL01);陕西省中医药管理局第二批中医药重点研究室建设项目(陕中医药发2018[32号]);陕西省中医体质与疾病防治重点实验室(陕科基发[2012]1号)。

摘　　要：糖皮质激素性骨质疏松症(glucocorticoid-induced osteoporosis,GIOP)由长期或过量应用糖皮质激素(glucocorticoid,GC)所导致,其发病与骨质疏松症(osteoporosis,OP)相比有其自身特点。基于细胞自噬与OP的相关研究,探讨自噬与GC及GIOP三者之间的关联性。研究发现,在GC导致GIOP形成的过程中,针对不同GC浓度、不同细胞(BMSC、OB、骨细胞、OC)等,通过不同信号通路介导的细胞自噬发挥着复杂作用。要依据自噬对骨形成的积极作用开展GIOP的相关治疗,需要考虑多因素,将自噬水平精确调控在一个相对稳态范围内。Glucocorticoid-induced osteoporosis(GIOP)caused by long-term or excessive use of glucocorticoid(GC)has its own characteristics in the disease development compared with osteoporosis(OP).Based on the research of autophagy and OP,the relationship between autophagy and GC and GIOP is discussed.In the process of GC induced GIOP formation,autophagy mediated by different signaling pathways plays a complex role in different GC concentrations and different cells(BMSC,OB,osteocytes,OC).In order to carry out the treatment of GIOP according to the positive effect of autophagy on bone formation,we need to consider multiple factors and accurately regulate the level of autophagy in a relatively stable range.

关 键 词：自噬 糖皮质激素 糖皮质激素性骨质疏松症 细胞 

分 类 号：R589.5[医药卫生—内分泌]