探讨AGES-RAGE轴诱导铁死亡调控成骨细胞在DOP中的分子机制
To explore the molecular mechanism of AGE-RAGE axis induced ferroptosis regulating osteoblasts in DOP
  
DOI:10.3969/j.issn.1006-7108.2025.06.015
中文关键词:  AGES-RAGE轴  铁死亡  成骨细胞  DOP
英文关键词:AGES-RAGE axis  ferroptosis  osteoblasts  DOP
基金项目: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)
作者单位
周小青1 马兰1 张亚静1 丁娟娟1 王晓晖2* 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 
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中文摘要:
      糖尿病骨质疏松症(diabetes osteoporosis, DOP)是由糖尿病诱发的继发性骨质疏松症,是由于长期碳水化合物以及脂肪、蛋白质、钙磷代谢紊乱而表现出不同程度的骨质流失、骨矿物质密度低、骨微结构退化以及骨脆性并随糖尿病持续存在而增加。随着全球人口逐渐老龄化,DOP的发病率也在逐年上升。研究表明晚期糖基化终产物(AGEs)及其膜受体RAGE可通过介导不同信号通路参与成骨细胞的调节,如高糖(HG)环境诱导下成骨细胞发生铁死亡。故本文主要以铁死亡为轴,对HG环境中异常表达的 AGES-RAGE 轴诱导铁死亡调控成骨细胞过程中的具体作用机制进行综述,为临床治疗本病提供新的靶点。
英文摘要:
      Diabetes osteoporosis (DOP) is a secondary osteoporosis induced by diabetes, which is caused by long-term carbohydrate, fat, protein, and osteoporosis. Calcium and phosphorus metabolism disorders show varying degrees of bone loss, low bone mineral density, bone microstructure degradation, and bone fragility, which increase with the persistence of diabetes.As the global population ages, the incidence of DOP is increasing year by year. Studies have shown that advanced glycation end products (AGEs) and their membrane receptor RAGE can participate in the regulation of osteoblasts through mediating different signaling pathways, such as Ferroptosis of osteoblasts induced by high glucose (HG) environment. Therefore, this paper mainly focused on Ferroptosis, and reviewed the specific mechanism of Ferroptosis regulation of osteoblasts induced by AGE-RAGE axis with abnormal expression in HG environment, providing a new target for clinical treatment of this disease.
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