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骨修复材料促成骨作用的分子机制

徐云容 唐梓闻 何飞

徐云容, 唐梓闻, 何飞. 骨修复材料促成骨作用的分子机制[J]. 昆明医科大学学报, 2023, 44(10): 168-179. doi: 10.12259/j.issn.2095-610X.S20231007
引用本文: 徐云容, 唐梓闻, 何飞. 骨修复材料促成骨作用的分子机制[J]. 昆明医科大学学报, 2023, 44(10): 168-179. doi: 10.12259/j.issn.2095-610X.S20231007
Yunrong XU, Ziwen TANG, Fei HE. Molecular Mechanisms of Osteogenesis Promoted by Bone Repair Materials[J]. Journal of Kunming Medical University, 2023, 44(10): 168-179. doi: 10.12259/j.issn.2095-610X.S20231007
Citation: Yunrong XU, Ziwen TANG, Fei HE. Molecular Mechanisms of Osteogenesis Promoted by Bone Repair Materials[J]. Journal of Kunming Medical University, 2023, 44(10): 168-179. doi: 10.12259/j.issn.2095-610X.S20231007

骨修复材料促成骨作用的分子机制

doi: 10.12259/j.issn.2095-610X.S20231007
基金项目: 国家自然科学基金资助项目(8216090283);云南省科技厅-昆明医科大学应用基础研究联合专项基金资助项目(202101AY070001-013)
详细信息
    作者简介:

    徐云容(1997~ ),男,云南曲靖人,在读硕士研究生,主要从事骨科基础研究工作

    何飞,1993年毕业于昆明医科大学,博士,主任医师,博士生导师。现任曲靖区域医疗中心院长,入选云南省云岭产业技术领军人才,云南省医学(骨科学)领军人才,云南省有突出贡献优秀专业技术人才,云南省中青年学术技术带头人,昆明市中青年学术技术带头人,享受云南省政府特殊津贴。担任教育部高等学校临床医学类专业指导委员会临床实践指导分委会委员等职。围绕干细胞与医用组织工程新材料和医学3D打印研究领域,先后主持国家自然科学基金2项、省级重大/重点等各类项目15项,累计科研经费达 2000余万元。以通讯作者、第一作者身份发表SCI收录论文、国家级核心期刊中英文论文45篇,主编专著6部,参编、参译8部,获得国家发明/实用新型专利/软件著作授权15项,获云南省科技进步三等奖2项,云南省卫生科技成果二等奖1项

    通讯作者:

    何飞,E-mail: 2115305737@qq.com

  • 中图分类号: R649.9

Molecular Mechanisms of Osteogenesis Promoted by Bone Repair Materials

  • 摘要: MAPK、PI3K/AKT、AMPK、TGF-β超家族、Wnt、Hippo、NF-κB、Notch、JAK/STAT、Hedgehog、整合素、OPG/RANKL/RANK、HIF等信号通路都与成骨分化相关,在骨修复材料促进成骨的过程中发挥着一定的调控作用,金属材料、无机材料、有机高分子材料和复合材料等骨修复材料可以通过激活一条或多条成骨相关信号通路促进骨组织再生。进一步了解骨修复材料促进成骨作用的相关分子机制将有助于骨修复材料更广泛地应用于骨组织工程和付诸临床实践,但目前关于骨修复材料促进成骨作用的具体分子机制还未彻底阐述清晰,未来仍需进一步研究。简要介绍现今与成骨分化相关的信号通路,综述骨修复材料在多种信号通路中的研究,为骨修复材料促成骨机制的深入研究提供借鉴。
  • 图  1  RTK通路、MAPK通路、PI3K/AKT通路、AMPK通路、整合素通路并行示意图

    箭头仅表示作用方向,MAPK为丝裂原活化蛋白激酶,MAPKK为MAPK激酶,MAPKKK为MAPKK激酶,FAK为局部黏着斑激酶,Ras为GTP结合蛋白Ras,Raf为丝/苏氨酸蛋白激酶Raf,MEK1/2/5为MAPK激酶1/2/5,ERK1/2/5为细胞外调节激酶1/2/5,Elk-1:细胞转录因子Elk-1,Traf6为泛素连接酶,Rac-1为GTP结合蛋白Rac-1,MEKK2/3/4为MAPKK激酶2/3/4,TAK1为转化生长因子β激酶1,MKK3/4/6/7为MAPK激酶3/4/6/7,JNK1/2/3为应激活化蛋白激酶1/2/3,MEF2:细胞转录因子MEF2,c-jun:细胞转录因子c-jun,GFs为各类生长因子,RTK为受体酪氨酸激酶,PI3K为磷脂酰肌醇3激酶,PIP2为磷脂酰肌醇2磷酸,PIP3为磷脂酰肌醇3磷酸,PDK1为三磷酸肌醇依赖性蛋白激酶1,AKT为蛋白激酶B,TSC1/2为GTP结合蛋白TSC1/2,mTORC1为哺乳动物雷帕霉素靶蛋白1,S6K为蛋白激酶S6K,4E-PB1为转录结合蛋白4E-PB1,GSK-3β为糖原合成酶激酶3β,FOXO为细胞转录因子FOXO,ACLY为ATP柠檬酸裂解酶,Ob-Rb为瘦素受体,CaMKK2为钙调蛋白依赖性蛋白激酶激酶2,LKB1为丝/苏氨酸激酶LKB1,AMPK为AMP依赖的蛋白激酶。

    Figure  1.  Parallel diagram of RTK pathway,MAPK pathway,PI3K/AKT pathway,AMPK pathway and integrin pathway

    图  2  TGF-β超家族信号通路示意图

    箭头仅表示作用方向,TGF-β为转化生长因子β,BMP为骨形态发生蛋白,AMH为抗缪勒管激素,Activin为激活素,GDF为生长分化因子,Smad1/2/3/4/5//6/7/8为磷酸化细胞信号转导分子1/2/3/4/5/6/7/8,P:磷酸化。

    Figure  2.  Schematic diagram of TGF-β superfamily signaling pathway

    图  3  Wnt/β-catenin信号通路示意图

    Figure  3.  Schematic diagram of Wnt/β-catenin signaling pathway

    图  4  NF-κB信号通路示意图

    A:NF-κB经典信号通路;B:NF-κB非经典信号通路。TNF-α为肿瘤坏死因子-α ,ILs为白介素,CD40L为白细胞分化抗原40配体,BAFF为B淋巴细胞活化因子,LT-β为淋巴毒素-β,TNFR1、TLR、CD40、BAFFR、LTβR分别为TNF-α、ILs、CD40L、BAFF、LT-β对应的受体,TAK1为转化生长因子-β激活激酶1 ,IKK为IκB激酶 ,IκBα为κB 抑制蛋白α,NIK为NF-κB诱导激酶。

    Figure  4.  Schematic diagram of | NF-κB signaling pathway

    表  1  复合材料成骨机制的研究

    Table  1.   Studies on osteogenic mechanism of composite materials

    研究者 发表年份 材料 生物相容性 信号通路
    LEE等[86] 2023 掺入了氧化锌/阿仑膦酸钠/BMP2纳米颗粒的细胞外基质/聚乳酸-羟基乙酸共聚物/改性后的氢氧化镁复合材料 良好 NO/cGMP和Wnt/β-catenin信号通路
    SHI等[77] 2022 聚己内酯/壳聚糖复合材料 良好 p38/MAPK和Hippo信号通路
    ZHANG等[78] 2022 甲基丙烯酰壳聚糖/β-磷酸三钙水凝胶 良好 Hippo信号通路
    WANG等[79] 2022 还原性谷胱甘肽接枝甲基丙烯酸明胶所制备的抗氧化水凝胶 良好 PI3K/AKT信号通路
    XUE等[80] 2022 壳聚糖季铵盐/氧化石墨烯/聚多巴胺复合材料 良好 BMP /Smads信号通路
    HUANG等[16] 2022 钽/钛合金 良好 ILK/ERK1/2信号通路
    JIA等[81] 2021 锌/锶合金 良好 Wnt/β-catenin、PI3K/AKT和MAPK/ERK信号通路
    YANG等[82] 2021 包含L-精氨酸和Ca2+的骨膜模拟助骨剂 良好 NO/cGMP信号通路
    CHENG等[83] 2021 聚乳酸-羟基乙酸共聚物 /β-磷酸三钙复合材料 良好 MAPK和PI3K/AKT信号通路
    ZOU等[85] 2021 负载甲状旁腺激素和纳米羟基磷灰石的壳聚糖/海藻酸钠水凝胶 良好 Notch信号通路
    FU等[84] 2019 硫化铋/羟基磷灰石薄膜包裹的钛 良好 Wnt/Ca2+信号通路
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