HMGB1介导TLR4/NF⁃κB信号通路干预骨关节炎研究进展
Research progress in the intervention of osteoarthritis by HMGB1 through TLR4/NF-κB signaling pathway
  
DOI:10.3969/j.issn.1006-7108.2023.10.021
中文关键词:  骨关节炎  HMGB1/TLR4/NF-κB信号通路  研究进展
英文关键词:osteoarthritis  HMGB1/TLR4/NF-κB signaling pathway  research progress
基金项目:兰州市科技发展指导性项目(2020-ZD-65);甘肃省青年科技基金(20JR10RA345);甘肃省卫生健康行业科研项目(GSWSKY-2021-009);兰州市城关区科技局(2020JSCX0065);甘肃中医药大学附属医院创新基金(gzfy-2020-24);甘肃省拔尖领军人才项目
作者单位
谢兴文1,2* 陈欣1,2 刘建军1 李元贞1 席芳琴1 齐伟2 闫文2 陈一新2 1.甘肃中医药大学附属医院,甘肃 兰州 730000 甘肃中医药大学,甘肃 兰州 730030 
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中文摘要:
      骨关节炎(osteoarthritis, OA)作为临床常见老年退行性疾病,目前尚无有效治疗手段。研究发现OA是一种慢性低度炎性疾病。损伤相关分子模式HMGB1(high mobility group box-1)在OA病理过程中发挥中心分子作用。HMGB1与固有免疫模式识别受体TLR4(toll-like receptor 4, TLR4)结合后激活NF-κB信号通路导致OA软骨退变和滑膜炎等免疫炎症反应。通过综述HMGB1介导TLR4/NF-κB信号通路在OA发病机制中的作用,为靶向阻断HMGB1治疗OA提供理论依据和参考。
英文摘要:
      Osteoarthritis (OA) is a common clinical degenerative disease, but there is no effective treatment at present. Studies have found that OA is a chronic low-grade inflammatory disease. Damage-related molecular pattern HMGB1 (high mobility group box-1) plays a central molecular role in the pathological process of OA. HMGB1 binds to Toll-like receptor (4TLR4), the innate immune pattern recognition receptor, and activates NF-κB signaling pathway, leading to OA cartilage degeneration and synovitis. This article reviews the role of HMGB1 mediated TLR4/NF-κB signaling pathway in the pathogenesis of OA, so as to provide theoretical basis and reference for the targeted blockade of HMGB1 in the treatment of OA.
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