骨膜蛋白在骨科疾病中的研究进展
DOI:
作者:
作者单位:

兰州大学第二医院

作者简介:

通讯作者:

中图分类号:

基金项目:

甘肃省自然科学基金(编号:2020-0405-JCC-1568)


Research progress of POSTN in bone degenerative diseases
Author:
Affiliation:

Lanzhou University Second Hospital

Fund Project:

Natural Science Foundation of Gansu Province (No.: 2020-0405-JCC-1568)

  • 摘要
  • |
  • 图/表
  • |
  • 访问统计
  • |
  • 参考文献
  • |
  • 相似文献
  • |
  • 引证文献
  • |
  • 资源附件
  • |
  • 文章评论
    摘要:

    骨膜蛋白(Periostin,POSTN)作为一种细胞外基质蛋白,在大多数正常组织、细胞中低水平表达,然而在病理性部位却高度表达。POSTN通过与细胞表面的整合素结合并激活Wnt/β-catenin、NF-κB等多条信号通路,导致疾病的发生发展。近年来研究发现POSTN在骨关节炎(Osteoarthritis,OA)的软骨细胞中高度表达,并通过促进其细胞外基质(Extracellular matrix,ECM)的降解和上调软骨细胞中的炎症因子,加速OA的进展。此外,最近的研究表明在退变的椎间盘细胞中POSTN也表达增加,POSTN可能是调控椎间盘退变(Intervertebral disc degeneration,IVDD)的关键因子。另外,POSTN还可以促进骨的形成、再生与修复,为骨质疏松提供新的治疗方向。本文就POSTN参与调控骨性退行性疾病的作用及机制进行综述。

    Abstract:

    Periostin (POSTN), as an extracellular matrix protein, is expressed at a low level in most normal tissues and cells, but highly expressed in pathological sites. POSTN leads to the occurrence and development of disease by binding to integrins on the cell surface and activating many signaling pathways such as Wnt/ β-catenin, NF- κ B and so on. In recent years, it has been found that POSTN is highly expressed in chondrocytes of osteoarthritis (OA), and accelerates the progress of OA by promoting the degradation of extracellular matrix (ECM) and up-regulating inflammatory factors in chondrocytes. Moreover, recent studies have shown that the expression of POSTN is also increased in degenerative intervertebral disc cells, and POSTN may be a key factor in the regulation of intervertebral disc degeneration (IVDD). In addition, POSTN can also promote bone formation, regeneration and repair, and provide a new direction for the treatment of osteoporosis. This article reviews the characteristic and mechanism of POSTN in the regulation of bone degenerative diseases.

    参考文献
    相似文献
    引证文献
引用本文
分享
文章指标
  • 点击次数:
  • 下载次数:
  • HTML阅读次数:
  • 引用次数:
历史
  • 收稿日期:2021-12-25
  • 最后修改日期:2022-03-07
  • 录用日期:2022-06-30
  • 在线发布日期:
  • 出版日期: