邮件订阅 RSS

留言板

尊敬的读者、作者、审稿人, 关于本刊的投稿、审稿、编辑和出版的任何问题, 您可以本页添加留言。我们将尽快给您答复。谢谢您的支持!

姓名
邮箱
手机号码
标题
留言内容
验证码

HMGB1在调节骨关节炎软骨细胞功能中的作用机制

齐鑫,  张晓刚,  陈欣,  安文博,  王志鹏,  王多贤,  罗鹏飞,  陈一新,  马姣姣,  齐伟,  胡紫阳,  刘建军

downloadPDF
文章导航 > 协和医学杂志  > 2023 > 优先出版
齐鑫, 张晓刚, 陈欣, 安文博, 王志鹏, 王多贤, 罗鹏飞, 陈一新, 马姣姣, 齐伟, 胡紫阳, 刘建军. HMGB1在调节骨关节炎软骨细胞功能中的作用机制[J]. 协和医学杂志. doi: 10.12290/xhyxzz.2023-0269
引用本文: 齐鑫, 张晓刚, 陈欣, 安文博, 王志鹏, 王多贤, 罗鹏飞, 陈一新, 马姣姣, 齐伟, 胡紫阳, 刘建军. HMGB1在调节骨关节炎软骨细胞功能中的作用机制[J]. 协和医学杂志. doi: 10.12290/xhyxzz.2023-0269
shu
QI Xin, ZHANG Xiaogang, CHEN Xin, AN Wenbo, WANG Zhipeng, WANG Duoxian, LUO Pengfei, CHEN Yixin, MA Jiaojiao, QI Wei, HU Ziyang, LIU Jianjun. Research Progress on the Role of HMGB1 in Regulating the Function of Osteoarthritis Chondrocytes[J]. Medical Journal of Peking Union Medical College Hospital. doi: 10.12290/xhyxzz.2023-0269
Citation: QI Xin, ZHANG Xiaogang, CHEN Xin, AN Wenbo, WANG Zhipeng, WANG Duoxian, LUO Pengfei, CHEN Yixin, MA Jiaojiao, QI Wei, HU Ziyang, LIU Jianjun. Research Progress on the Role of HMGB1 in Regulating the Function of Osteoarthritis Chondrocytes[J]. Medical Journal of Peking Union Medical College Hospital. doi: 10.12290/xhyxzz.2023-0269
shu

HMGB1在调节骨关节炎软骨细胞功能中的作用机制

doi: 10.12290/xhyxzz.2023-0269

  • 1 甘肃中医药大学, 兰州 730000;

  • 2 甘肃中医药大学附属医院, 兰州 730000

基金项目: 

张晓刚全国名老中医药专家传承工作室建设项目（国中医药人教函[2022]75号）；甘肃省自然科学基金（23JRRA1192）；2020年兰州市人才创新创业项目（2020-RC-64）；甘肃省教育厅高等学校创新基金（2022B-109）；2020年甘肃省青年科技基金（20JRTORA345）；兰州市城关区科技计划项目（2020-2-2-7）；2021年卫生健康行业科研项目（GSWSKY-2021-069）；2021年度甘肃省中医药科研课题项目（GZKP-2021-16）；甘肃中医药大学研究生创新基金

详细信息
    通讯作者:

    刘建军，E-mail：g.sljj@163.com

  • 中图分类号: R684.3； G612

Research Progress on the Role of HMGB1 in Regulating the Function of Osteoarthritis Chondrocytes

  • 1 Gansu University of Traditional Chinese Medicine, Lanzhou 730000, China;

  • 2 Affiliated Hospital of Gansu University of Traditional Chinese Medicine, Lanzhou 730000, China

Funds: 

Zhang Xiaogang National Famous Traditional Chinese Medicine Expert Inheritance Studio Construction Project (National Traditional Chinese Medicine Human Education Letter [2022] No. 75); Gansu Provincial Natural Science Foundation Project (23JRRA1192); 2020 Lanzhou Talent Innovation and Entrepreneurship Project (2020-RC-64)); Gansu Provincial Department of Education College Innovation Fund Project (2022B-109); 2020 Gansu Provincial Youth Science and Technology Fund (20JRTORA345); Lanzhou City Chengguan District Science and Technology Plan Project (2020-2-2-7); 2021 Health Industry Scientific research project (GSWSKY-2021-069); 2021 Gansu Province Traditional Chinese Medicine Scientific Research Project (GZKP-2021-16); Gansu University of Traditional Chinese Medicine Graduate Student Innovation and Entrepreneurship Project

    摘要
  • 摘要: 骨关节炎（osteoarthritis，OA）是一种慢性退行性关节疾病，其主要特征是关节软骨破坏，导致患者身体疼痛和残疾，严重影响患者生活质量。OA可由多种病因诱发，而关节软骨的病理改变被认为是OA发生的关键驱动因素之一。高迁移率族蛋白1（high mobility group box-1 protein，HMGB1）作为一种真核细胞内的非组蛋白，可参与调节软骨细胞炎症及凋亡过程，从而导致关节软骨受损，诱发OA。本文就HMGB1在OA软骨细胞中的作用机制研究进行综述，以期为临床防治OA提供新思路。
    Abstract: Osteoarthritis (OA) is a chronic degenerative joint disease whose main characteristic is the destruction of articular cartilage, causing pain and disability in patients and seriously affecting their quality of life. OA can be induced by a variety of causes, and pathological changes in articular cartilage are considered to be one of the key driving factors for the occurrence of OA. High mobility group box-1 protein (HMGB1), as a non-histone protein in eukaryotic cells, can participate in regulating the inflammation and apoptosis process of OA chondrocytes, thus leading to the occurrence of OA. This article reviews the research on the mechanism of HMGB1 in OA chondrocytes, with a view to providing new ideas for the clinical prevention and treatment of OA.
    • HTML全文
    • 参考文献(43)
  • [1] 褚云峰, 于红燕, 杨琪, 等. 白藜芦醇在骨关节炎中的作用及机制研究进展[J]. 中国骨质疏松杂志, 2022, 28:1351-1355.
    [2] Lubbers R, van Schaarenburg RA, Kwekkeboom JC, et al. Complement component C1q is produced by isolated articular chondrocytes[J]. Osteoarthritis Cartilage, 2020, 28:675-684.
    [3] Liu Z, Zhang H, Wang H, et al. Magnolol Alleviates IL-1beta-Induced Dysfunction of Chondrocytes Through Repression of SIRT1/AMPK/PGC-1alpha Signaling Pathway[J]. J Interferon Cytokine Res, 2020, 40:145-151.
    [4] 杨昊. Navitoclax(ABT263)改善骨关节炎中炎症微环境和减轻软骨破坏的研究[D]. 中国人民解放军陆军军医大学, 2021. doi: 10.27001/d.cnki.gtjyu.2020.

    000249.
    [5] Colavita L, Ciprandi G, Salpietro A, et al. HMGB1:A pleiotropic activity[J]. Pediatr Allergy Immunol, 2020, 31 Suppl 26(Suppl 26):63-65.
    [6] Chen R, Kang R, Tang D. The mechanism of HMGB1 secretion and release[J]. Exp Mol Med, 2022, 54:91-102.
    [7] Dong Y, Ming B, Dong L. The Role of HMGB1 in Rheumatic Diseases[J]. Front Immunol, 2022, 13:815257.
    [8] 王晓艳, 杜虹. 高迁移率族蛋白B1在脓毒症和创伤后炎症反应中的作用[J]. 微生物学免疫学进展, 2020, 48:79-83.
    [9] Xue J, Suarez JS, Minaai M, et al. HMGB1 as a therapeutic target in disease[J]. J Cell Physiol, 2021, 236:3406-3419.
    [10] Motta F, Barone E, Sica A, et al. Inflammaging and Osteoarthritis[J]. Clin Rev Allergy Immunol, 2023, 64:222-238.
    [11] Ma W, Wang X, Wang C, et al. Up-regulation of P21-activated kinase 1 in osteoarthritis chondrocytes is responsible for osteoarthritic cartilage destruction[J]. Biosci Rep, 2020, 40:BSR20191017.
    [12] 唐丹, 王先斌, 杨香莲, 等. 跑台运动训练对脊髓损伤后大鼠肺损伤及HMGB1/TLR4/NF-κ B信号通路表达的影响[J]. 中国康复医学杂志, 2023, 38:159-166.
    [13] Zhang C, Yu W, Huang C, et al. Chrysin protects human osteoarthritis chondrocytes by inhibiting inflammatory mediator expression via HMGB1 suppression[J]. Mol Med Rep, 2019, 19:1222-1229.
    [14] Wang Y, Shen S, Li Z, et al. MIR-140-5p affects chondrocyte proliferation, apoptosis, and inflammation by targeting HMGB1 in osteoarthritis[J]. Inflamm Res, 2020, 69:63-73.
    [15] Wen ZL, Jiangdong N, Deye S, et al. Dual regulatory roles of HMGB1 in inflammatory reaction of chondrocyte cells and mice[J]. Cell Cycle, 2019, 18:2268-2280.
    [16] Yang H, Wang H, Andersson U. Targeting Inflammation Driven by HMGB1[J]. Front Immunol, 2020, 11:484.
    [17] Jimi E, Fei H, Nakatomi C. NF-kappaB Signaling Regulates Physiological and Pathological Chondrogenesis[J]. Int J Mol Sci, 2019, 20:6275.
    [18] Zhong H, Li X, Zhou S, et al. Interplay between RAGE and TLR4 Regulates HMGB1-Induced Inflammation by Promoting Cell Surface Expression of RAGE and TLR4[J]. J Immunol, 2020, 205:767-775.
    [19] Meng Y, Qiu S, Sun L, et al. Knockdown of exosome-mediated lnc-PVT1 alleviates lipopolysaccharide-induced osteoarthritis progression by mediating the HMGB1/TLR4/NF- kappaB pathway via miR-93-5p[J]. Mol Med Rep, 2020, 22:5313-5325.
    [20] Hu SL, Wang K, Shi YF, et al. Downregulating Akt/NF-kappaB signaling and its antioxidant activity with Loureirin A for alleviating the progression of osteoarthritis:In vitro and vivo studies[J]. Int Immunopharmacol, 2020, 78:105953.
    [21] Hu Z, Xiao M, Cai H, et al. Glycyrrhizin regulates rat TMJOA progression by inhibiting the HMGB1-RAGE/TLR4-NF-kappaB/AKT pathway[J]. J Cell Mol Med, 2022, 26:925-936.
    [22] Romerio A, Peri F. Increasing the Chemical Variety of Small-Molecule-Based TLR4 Modulators:An Overview[J]. Front Immunol, 2020, 11:1210.
    [23] Li C, He Y, Li Y, et al. A novel method to establish the rabbit model of knee osteoarthritis:intra-articular injection of SDF-1 induces OA[J]. BMC Musculoskelet Disord, 2021, 22:329.
    [24] Xiang Y, Li Y, Yang L, et al. miR-142-5p as a CXCR4-Targeted MicroRNA Attenuates SDF-1-Induced Chondrocyte Apoptosis and Cartilage Degradation via Inactivating MAPK Signaling Pathway[J]. Biochem Res Int, 2020, 2020:4508108.
    [25] Liang S, Lv ZT, Zhang JM, et al. Necrostatin-1 Attenuates Trauma-Induced Mouse Osteoarthritis and IL-1beta Induced Apoptosis via HMGB1/TLR4/SDF-1 in Primary Mouse Chondrocytes[J]. Front Pharmacol, 2018, 9:1378.
    [26] Zhang J, Cheng F, Rong G, et al. Hsa_circ_0005567 Activates Autophagy and Suppresses IL-1beta-Induced Chondrocyte Apoptosis by Regulating miR-495[J]. Front Mol Biosci, 2020, 7:216.
    [27] Gao Y, Zhao H, Li Y. LncRNA MCM3AP-AS1 regulates miR-142-3p/HMGB1 to promote LPS-induced chondrocyte apoptosis[J]. BMC Musculoskelet Disord, 2019, 20:605.
    [28] Qiu M, Liu D, Fu Q. MiR-129-5p shuttled by human synovial mesenchymal stem cell-derived exosomes relieves IL-1beta induced osteoarthritis via targeting HMGB1[J]. Life Sci, 2021, 269:118987.
    [29] Pan H, Dai H, Wang L, et al. MicroRNA-410-3p modulates chondrocyte apoptosis and inflammation by targeting high mobility group box 1(HMGB1) in an osteoarthritis mouse model[J]. BMC Musculoskelet Disord, 2020, 21:486.
    [30] Lin J, Song T, Li C, et al. GSK-3beta in DNA repair, apoptosis, and resistance of chemotherapy, radiotherapy of cancer[J]. Biochim Biophys Acta Mol Cell Res, 2020, 1867:118659.
    [31] Yuan X, Li L, Shi W, et al. TMF protects chondrocytes from ER stress-induced apoptosis by down-regulating GSK-3beta[J]. Biomed Pharmacother, 2017, 89:1262-1268.
    [32] Ba C, Ni X, Yu J, et al. Ubiquitin conjugating enzyme E2 M promotes apoptosis in osteoarthritis chondrocytes via Wnt/beta-catenin signaling[J]. Biochem Biophys Res Commun, 2020, 529:970-976.
    [33] Sun Y, Wang F, Sun X, et al. CX3CR1 regulates osteoarthrosis chondrocyte proliferation and apoptosis via Wnt/beta-catenin signaling[J]. Biomed Pharmacother, 2017, 96:1317-1323.
    [34] Shu Z, Miao X, Tang T, et al. The GSK-3beta/beta-catenin signaling pathway is involved in HMGB1-induced chondrocyte apoptosis and cartilage matrix degradation[J]. Int J Mol Med, 2020, 45:769-778.
    [35] 廖建青, 马富文, 张英杰, 等. 骨痹合剂对膝关节骨性关节炎原代软骨细胞PI3K/AKT信号通路的影响[J]. 中华中医药杂志, 2022, 37:2322-2326.
    [36] Shi X, Jie L, Wu P, et al. Calycosin mitigates chondrocyte inflammation and apoptosis by inhibiting the PI3K/AKT and NF-kappaB pathways[J]. J Ethnopharmacol, 2022, 297:115536.
    [37] Li D, Ni S, Miao KS, et al. PI3K/Akt and caspase pathways mediate oxidative stress-induced chondrocyte apoptosis[J]. Cell Stress Chaperones, 2019, 24:195-202.
    [38] 习洋. 生长分化因子-11(GDF11)通过抑制MAPK和PI3K-AKT/NF-κ B通路发挥抗骨关节炎作用的体内外研究[D]. 华中科技大学, 2020. doi: 10.27157/d.cnki.ghzku.2020.

    003129.
    [39] Bigeard J, Hirt H. Nuclear Signaling of Plant MAPKs[J]. Front Plant Sci, 2018, 9:469.
    [40] 张传成, 沈美花, 陈利锋. 氧化应激调控MAPK信号通路与骨关节炎治疗研究进展[J]. 中国骨质疏松杂志, 2023, 29:583-588.
    [41] 傅永升, 谭茗月, 王卫国, 等. 中药调控膝骨关节炎相关信号通路的研究进展[J]. 中国实验方剂学杂志, 2023:1-17.
    [42] Zhou Y, Ming J, Li Y, et al. Ligustilide attenuates n itric oxide-induced apoptosis in rat chondrocytes and cartilage degradation via inhibiting JNK and p38 MAPK pathways[J]. J Cell Mol Med, 2019, 23:3357-3368.
    [43] Huang X, Xi Y, Mao Z, et al. Vanillic acid attenuates cartilage degeneration by regulating the MAPK and PI3K/AKT/NF-kappaB pathways[J]. Eur J Pharmacol, 2019, 859:172481.
    • 相关文章
    • 施引文献
  • 资源附件(0)
  • 加载中
WeChat 点击查看大图
计量
  • 文章访问数:  16
  • HTML全文浏览量:  3
  • PDF下载量:  5
  • 被引次数: 0
出版历程
  • 收稿日期:  2023-06-05
  • 录用日期:  2023-08-11
  • 网络出版日期:  2023-11-20

目录

    /

    返回文章
    返回
    友情链接: 国家卫生健康委员会 北京协和医院 中国医学科学院 学术不端检测系统 国际知识资源总库 中国知网 术语在线 中国全科医学
    地址：北京市东城区帅府园1号 北京协和医院老楼7号楼
    3层302室 《协和医学杂志》编辑部
    电话：010-69154261/4262
    E - mail：medj@pumch.cn
    mjpumch@126.com
    期刊网站版权所有：《协和医学杂志》编辑部
    京ICP备 11002662

    本系统由 北京仁和汇智信息技术有限公司 开发    百度统计

    x 关闭 永久关闭

    【温馨提醒】近日，《协和医学杂志》编辑部接到作者反映，有多名不法人员冒充期刊编辑发送见刊通知，鼓动作者添加微信，从而骗取版面费的行为。特提醒您，本刊与作者联系的方式均为邮件通知或电话，稿件进度通知邮箱为：mjpumch@126.com，编辑部电话为：010-69154261，请提高警惕，谨防上当受骗！如有任何疑问，请致电编辑部核实。谢谢！