NLRP3介导细胞焦亡在糖尿病性骨质疏松症中作用机制  

The mechanism of NLRP3-mediated pyrodeath in diabetic osteoporosis

作　　者：丁娟娟 张亚静 马兰[1,2] 周小青 王晓晖 DING Juanjuan;ZHANG Yajing;MA Lan;ZHOU Xiaoqing;WANG Xiaohui(Gansu University of Traditional Chinese Medicine,Lanzhou 730030,China;Gansu Provincial Hospital of Traditional Chinese Medicine,Lanzhou 730050,China)

机构地区：[1]甘肃中医药大学,甘肃兰州730030 [2]甘肃省中医院,甘肃兰州730050

出　　处：《中国骨质疏松杂志》2025年第2期255-260,共6页Chinese Journal of Osteoporosis

基　　金：国家中医优势专科建设项目[甘卫中医函(2023)63号];甘肃省科技重点研发计划项目(21YF5FA022);兰州市人才创新创业项目(2021-RC-118);甘肃省中医药项目(GZKZ-2024-8)。

摘　　要：细胞焦亡被定义为程序性死亡,其特征是细胞肿胀直至细胞膜破裂、细胞内容物释放并激活强烈的炎症反应。糖尿病性骨质疏松症(diabetic osteoporosis,DOP)是糖尿病相关并发症的一种,表现为骨密度降低、骨量减少和骨结构异常,显著增加了骨折风险。越来越多的研究揭示,在DOP中,成骨细胞由于各种因素的影响,释放了如NOD样受体热蛋白结构域蛋白3(NOD like receptor protein structure domain protein 3,NLRP3)和白细胞介素(IL-1β、IL-18)等媒介物,这些媒介物活化既可以导致细胞焦亡,又在破骨细胞过度分化及骨质疏松症发生中扮演着关键角色。本综述旨在总结细胞焦亡在DOP中的研究进展,并探讨其作为一种潜在的治疗靶点的可能性。Cell pyroptosis is defined as programmed death,leading to cell swelling until membrane rupture,release of cell contents,and activation of a strong inflammatory response.Diabetic Osteoporosis(DOP)is a complication of diabetes mellitus,which is characterized by decreased bone mineral density,decreased bone mass,and abnormal bone structure,significantly increasing the risk of fracture.A growing body of research has revealed that in the DOP,osteoblast due to the influence of various factors,released as heat NOD like receptor protein structure domain protein 3(NLRP3)and interleukin(IL-1 beta,IL-18)such as vehicle,the vehicle can lead to cell activation jiao wu,It also plays a key role in the excessive differentiation of osteoclasts and the occurrence of osteoporosis.The aim of this review is to summarize the research progress of pyroptosis in DOP and to explore the possibility of pyroptosis as a potential therapeutic target.

关 键 词：糖尿病性骨质疏松症 焦亡 NOD样受体热蛋白结构域蛋白3(NLRP3) 信号通路 治疗 

分 类 号：R587.2[医药卫生—内分泌]