摘要
目的对近年来脂肪细胞因子在椎间盘退变(intervertebral disc degeneration,IVDD)过程中的作用及其机制的研究进展进行综述。方法广泛查阅近年国内外与脂肪细胞因子在IVDD过程中作用研究有关的文献,对脂肪细胞因子种类及功能、在IVDD过程中的作用及机制,以及在椎间盘生物治疗中的应用前景进行总结。结果脂肪细胞因子是一种主要由脂肪组织分泌的生物活性物质,在骨关节疾病、代谢性疾病、乳腺癌等疾病中具有重要作用。在IVDD过程中,多数脂肪细胞因子通过与自身受体结合来激活多种信号传导途径,引起椎间盘内细胞增殖及凋亡失调、促炎及抗炎因子分泌紊乱,进而导致椎间盘内代谢失衡和初始炎症环境的建立。结论脂肪细胞因子作为一种具有代谢和免疫调节功能的生物活性物质,在IVDD的发生、发展及生物治疗等方面发挥着重要作用。
Objective To review the research progress of the role and mechanism of adipokines in intervertebral disc degeneration(IVDD) in recent years. Methods The domestic and foreign literature related to adipokines in the process of IVDD was extensively reviewed. The types and functions of adipokines, the role and mechanism in the process of IVDD, and the application prospects of intervertebral disc biotherapy were reviewed. Results As a kind of bioactive substance secreted by adipose tissue, adipokine plays an important role in bone and joint diseases, metabolic diseases, and breast cancer. During IVDD, most adipokines can activate multiple signaling pathways by binding to autoreceptors, cause the proliferation and apoptosis of cells and proinflammatory and anti-inflammatory factors parasecretions in the intervertebral disc, and lead to imbalance of intradiscal metabolism and establishment of the initial inflammatory environment, and finally cause the IVDD. Conclusion Adipokines, as a biologically active substance with metabolic and immunomodulatory functions, play important roles in the occurrence, development, and biological treatment of IVDD.
作者
巩朝阳
赵光海
向高
刘开鑫
张海鸿
GONG Chaoyang;ZHAO Guanghai;XIANG Gao;LIU Kaixin;ZHANG Haihong(Department of Orthopedics,Lanzhou University Second Hospital,Gansu Key Laboratory of Bone and Joint Diseases,Lanzhou Gansu,730000,P.R.China)
出处
《中国修复重建外科杂志》
CAS
CSCD
北大核心
2020年第3期399-403,共5页
Chinese Journal of Reparative and Reconstructive Surgery
基金
甘肃省自然科学基金资助项目(CY2017-MS06)
国家自然科学基金资助项目(31960175)。
关键词
脂肪细胞因子
椎间盘退变
炎症反应
生物治疗
Adipokine
intervertebral disc degeneration
inflammatory response
biotherapy
作者简介
通信作者:张海鸿,Email:zhanghaihong1968@sina.com。
