OPG-RANKL-RANK轴介导P38 MAPK信号通路调控破骨细胞在糖尿病性骨质疏松症中的作用研究进展
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作者单位:

1.甘肃中医药大学,甘肃 兰州 730030;2.甘肃省中医院 糖尿病科,甘肃 兰州 730050

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通讯作者:

王晓晖,E-mail:997869467@qq.com;Tel:13893390965

中图分类号:

R587.2

基金项目:

国家中医优势专科建设项目(No: 甘卫中医函〔2023〕63号);甘肃省科技重点研发计划项目(No: 21YF5FA022);兰州市人才创新创业项目(No: 2021-RC-118)


Research progress on the role of the OPG-RANKL-RANK axis in regulating osteoclasts in diabetic osteoporosis via the P38 MAPK signaling pathway
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Affiliation:

1.Gansu University of Traditional Chinese Medicine, Lanzhou, Gansu 730030, China;2.Department of Diabetes, Gansu Provincial Hospital of Traditional Chinese Medicine, Lanzhou, Gansu 730050, China

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    摘要:

    糖尿病性骨质疏松症(DOP)是糖尿病在骨骼系统中最常见的慢性并发症。DOP起病隐匿,症状不典型,在疾病早期容易被忽视,致残率和致死率较高。已有研究发现OPG-RANKL-RANK轴是调节破骨细胞分化成熟和骨吸收的关键因子,可通过介导不同的信号通路调节骨代谢,如调控破骨细胞生成分化的P38 MAPK信号通路,因此,进一步研究了解OPG-RANKL-RANK轴与P38 MAPK信号通路的关系可为DOP的防治提供新思路。该文综述OPG-RANKL-RANK轴介导P38 MAPK信号通路调控破骨细胞在DOP中的作用机制,为临床治疗DOP提供新的研究方向。

    Abstract:

    Diabetic osteoporosis (DOP) is the most common chronic complication of diabetes in the skeletal system. DOP is often insidious in onset, with atypical symptoms, which makes it easy to be overlooked in the early stages. Its disability and mortality rates are relatively high. Studies have shown that the OPG-RANKL-RANK axis is a key factor in regulating osteoclast differentiation, maturation, and bone resorption. This axis can modulate bone metabolism by mediating various signaling pathways, including the P38 MAPK signaling pathway, which regulates osteoclastogenesis and differentiation. Therefore, further exploration of the relationship between the OPG-RANKL-RANK axis and the P38 MAPK signaling pathway could provide new insights for the prevention and treatment of DOP. This review summarizes the mechanisms through which the OPG-RANKL-RANK axis mediates the P38 MAPK signaling pathway to regulate osteoclasts in DOP, offering new research directions for clinical treatment.

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马兰,王晓晖,周小青,马桃梅,韩世杰,丁娟娟,张亚静. OPG-RANKL-RANK轴介导P38 MAPK信号通路调控破骨细胞在糖尿病性骨质疏松症中的作用研究进展[J].中国现代医学杂志,2025,35(1):47-53

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  • 收稿日期:2024-07-10
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  • 在线发布日期: 2025-03-19
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