Interleukin-1β in intervertebral disk degeneration

被引:114
作者
Yang, Wei [1 ]
Yu, Xiao-Hua [2 ]
Wang, Cheng [1 ]
He, Wen-Si [1 ]
Zhang, Shu-Jun [1 ]
Yan, Yi-Guo [1 ]
Zhang, Jian [3 ]
Xiang, Yong-Xiao [3 ]
Wang, Wen-Jun [1 ]
机构
[1] Univ South China, Affiliated Hosp 1, Dept Spine Surg, Hengyang 421001, Hunan, Peoples R China
[2] Univ South China, Life Sci Res Ctr, Hengyang 421001, Hunan, Peoples R China
[3] Univ South China, Affiliated Hosp 1, Dept Hand & Microsurg, Hengyang 421001, Hunan, Peoples R China
基金
中国国家自然科学基金;
关键词
IL-1; IDD; Inflammatory responses; Angiogenesis; Apoptosis; NUCLEUS PULPOSUS CELLS; TUMOR-NECROSIS-FACTOR; ANNULUS FIBROSUS CELLS; PLATELET-RICH PLASMA; P38 MAPK INHIBITION; LOW-BACK-PAIN; MATRIX METALLOPROTEINASES; IN-VITRO; OXIDATIVE STRESS; GENE-THERAPY;
D O I
10.1016/j.cca.2015.08.029
中图分类号
R446 [实验室诊断]; R-33 [实验医学、医学实验];
学科分类号
100118 [医学信息学]; 100208 [临床检验诊断学];
摘要
Intervertebral disk degeneration (IDD) is the most common diagnosis in patients with low back pain, a main cause of musculoskeletal disability in the world. Interleukin-1 (IL-1) beta is the most important member of the IL-1 family, and has a strong pro-inflammatory activity by stimulating the secretion of multiple pro-inflammatory mediators. IL-1 beta is highly expressed in degenerative intervertebral disk (IVD) tissues and cells, and it has been shown to be involved in multiple pathological processes during disk degeneration, including inflammatory responses, matrix destruction, angiogenesis and innervation, cellular apoptosis, oxidative stress and cellular senescence. However, inhibition of IL-1 beta is found to promote extracellular matrix (ECM) repair and protect against disk regeneration. In this review, after a brief description of IL-1 beta signaling, we mainly focus on the expression profiles, roles and therapeutic potential of IL-1 beta in IDD. A better understanding will help develop novel IL-1 beta-based therapeutic interventions for degenerative disk disease. (C) 2015 Elsevier B.V. All rights reserved.
引用
收藏
页码:262 / 272
页数:11
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