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
  
DOI:10.3969/j.issn.1006-7108.2025.02.015
中文关键词:  晚期糖基化终末产物  肌少-骨质疏松症  肌骨稳态  作用机制
英文关键词:advancedglycation end products  oligenia-osteoporosis  muscle bone homeostasis  mechanism of action
基金项目: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)
作者单位
孙兴翔1 孔令俊2* 邓叶龙1 李想1 张金磊1 韩升龙2 孟汉杰1 王植帅1 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 
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中文摘要:
      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。
英文摘要:
      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".
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