晚期糖基化终末产物在肌骨衰减疾病中作用机制  

The mechanism of advanced glycation end products in musculoskeletal attenuation disease

作　　者：孙兴翔 孔令俊[2] 邓叶龙 李想 张金磊 韩升龙 孟汉杰 王植帅 SUN Xingxiang;KONG Lingjun;DENG Yelong;LI Xiang;ZHANG Jinlei;HAN Shenglong;MENG Hanjie;WANG Zhishuai(Gansu University of Traditional Chinese Medicine,Lanzhou 730000,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730000 [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249-254,共6页Chinese Journal of Osteoporosis

基　　金：甘肃省中医院横向课题(20180401);兰州市科技计划项目(2023-2-20);兰州市科技计划项目(2023-ZD-49);甘肃省联合科研基金(24JRRA902)。

摘　　要：晚期糖基化终末产物(advanced glycation end products,AGEs)是脂质、蛋白质及核酸等物质与还原糖游离羰基之间经过氧化、脱水、缩合、异构化及环化等反应后形成的稳定糖基化产物,可参与诸多老年代谢性疾病调控。近年来随着对高糖诱导AGEs研究与探索的不断深入,发现其与维持“肌骨稳态”紧密关联,并参与肌骨衰减疾病的形成与发展。肌少-骨质疏松症(osteosarcopenia,OS)是以骨密度及肌肉质量、功能出现病理性丢失为特征且严重威胁老年人身心健康的一种老年代谢性疾病;易致老年人发生脆性骨折、残疾甚至死亡等不良后果。因此,本文对相关文献研究进行梳理,探讨高糖诱导下AGEs通过干预N6-甲基腺苷、DNA甲基化、自噬、铁死亡、RANKL/RANK通路、太空微重力环境、RAGE/AGEs通路、糖化交联等多类因素对肌少-骨质疏松症的影响,旨在探明高糖诱导的AGEs干预肌少-骨质疏松症的作用机制,以期为调控“肌骨稳态”提供新思路。Advanced glycation end products(AGEs)are stable glycosylation products formed after oxidation,dehydration,condensation,isomerization and cyclization between lipids,proteins,nucleic acids and free groups of reduced sugars,which can participate in the regulation of many metabolic diseases in the elderly.In recent years,with the deepening of the research and exploration of high glucose-induced AGEs,it is found that it is closely related to the maintenance of"muscle bone homeostasis"and participates in the formation and development of myosseous attenuation diseases.Sarcopenia-osteoporosis(osteosarcopenia,OS)is a senile metabolic disease characterized by bone density,pathological loss of muscle mass and function,which seriously threatens the physical and mental health of the elderly;which is prone to fragility fracture,disability and even death.Therefore,this paper discusses the effects of AGEs on sarcopenia-osteoporosis through N6-methyadenosine,DNA methylation,autophagy,iron death,RANKL/RANK pathway,space microgravity pathway,RAGE/AGEs pathway,glycan crosslinking,aiming to explore the mechanism of high glucose-induced AGEs in intervening sarcopenia-osteoporosis,in order to provide new ideas for regulating“muscle bone homeostasis”.

关 键 词：晚期糖基化终末产物 肌少-骨质疏松症 肌骨稳态 作用机制 

分 类 号：R681[医药卫生—骨科学]