文献类型：期刊文献

中文题名：由“伏毒-巨噬细胞极化-微炎症状态”路径探讨OP研究

英文题名：Research progress of OP was discussed based on the path of“Fudu-macrophage polarization-microinflammatory state”

作者：李平顺[1,2];王佳[2];田杰祥[2];周孟茹[2];王钢[2]

第一作者：李平顺

机构：[1]甘肃中医药大学,甘肃兰州730000;[2]甘肃中医药大学附属医院,甘肃兰州730000

第一机构：甘肃中医药大学

年份：2025

卷号：31

期号：2

起止页码：222

中文期刊名：中国骨质疏松杂志

外文期刊名：Chinese Journal of Osteoporosis

收录：;北大核心:【北大核心2023】；

基金：国家自然科学基金项目(81860858;81960832);甘肃省自然科学基金(22JR11RA133);甘肃中医药大学第二附属医院青年项目(ZX-62000004-2022-092);甘肃省名中医传承工作室建设项目[国中医药规财函(2021)50号];甘肃省科技计划项目(21JR11RA159)。

语种：中文

中文关键词：伏毒;巨噬细胞极化;微炎症状态;骨质疏松症

外文关键词：hypotoxic;macrophage polarization;microinflammatory state;osteoporosis

摘要：全世界有数亿人患有骨质疏松症,这会导致骨骼脆弱并增加骨折的风险。骨质疏松症与成骨抑制和破骨细胞生成增强密切相关。此外,微炎症状态和巨噬细胞极化也可能导致骨质疏松症。巨噬细胞对炎症反应至关重要,在微环境的控制下表现出不同的表型,其有两种主要的表型即经典巨噬细胞极化(M1型)和替代巨噬细胞极化(M2型)。一般来说,M1巨噬细胞主要导致骨吸收,而M2巨噬细胞则引起骨生成。M1/M2比值反映了巨噬细胞极化的“流动”状态,M1/M2比值失衡可能导致骨质疏松症等疾病。本综述以“伏毒”理论为切入点,以“伏毒-巨噬细胞极化-微炎症状态”路径为基础,旨在为骨质疏松症发病机制和潜在治疗靶点提供新见解。
Hundreds of millions of people around the world suffer from osteoporosis,which can lead to weak bones and an increased risk of fractures.Osteoporosis is closely related to osteogenic inhibition and osteoclast enhancement.In addition,microinflammatory states and macrophage polarization may also lead to osteoporosis.Macrophages are critical to the inflammatory response and exhibit different phenotypes under the control of the microenvironment.There are two main phenotypes,classical macrophage polarization(M1 type)and alternative macrophage polarization(M2 type).In general,M1 macrophages mainly cause bone resorption,while M2 macrophages cause bone formation.The M1/M2 ratio reflects the"fluid"state of macrophage polarization,and an imbalance of the M1/M2 ratio may lead to diseases such as osteoporosis.This review provides new insights into the pathogenesis and potential therapeutic targets of OP based on the"volvotoxic"theory and the"volvovirus-macrophage polarization-microinflammatory state"pathway.