TGF-β signaling in intervertebral disc health and disease

被引：132
作者：
Chen, S. [1 ]
Liu, S. [1 ]
Ma, K. [1 ]
Zhao, L. [1 ]
Lin, H. [1 ]
Shao, Z. [1 ]
机构：
[1] Huazhong Univ Sci & Technol, Union Hosp, Dept Orthopaed, Tongji Med Coll, Wuhan 430022, Hubei, Peoples R China
来源：
OSTEOARTHRITIS AND CARTILAGE | 2019年 / 27卷 / 08期
基金：
中国国家自然科学基金;
关键词：
Transforming growth factor-beta; Intervertebral disc; Nucleus pulposus; Degeneration; NUCLEUS PULPOSUS CELLS; GROWTH-FACTOR-BETA; ACTIVATED PROTEIN-KINASE; ANNULUS FIBROSUS CELLS; MESENCHYMAL STEM-CELL; TNF-ALPHA; EXTRACELLULAR-MATRIX; EMBRYONIC-DEVELOPMENT; UP-REGULATION; EXPRESSION;
D O I：
10.1016/j.joca.2019.05.005
中图分类号：
R826.8 [整形外科学]; R782.2 [口腔颌面部整形外科学]; R726.2 [小儿整形外科学]; R62 [整形外科学（修复外科学）];
学科分类号：
摘要：
Objective: This paper aims to provide a comprehensive review of the changing role of transforming growth factor-beta (TGF-beta) signaling in intervertebral disc (IVD) health and disease. Methods: A comprehensive literature search was performed using PubMed terms 'TGF-b' and 'IVD'. Results: TGF-beta signaling is necessary for the development and growth of IVD, and can play a protective role in the restoration of IVD tissues by stimulating matrix synthesis, inhibiting matrix catabolism, inflammatory response and cell loss. However, excessive activation of TGF-beta signaling is detrimental to the IVD, and inhibition of the aberrant TGF-beta signaling can delay IVD degeneration. Conclusions: Activation of TGF-beta signaling has a promising treatment prospect for IVD degeneration, while excessive activation of TGF-beta signaling may contribute to the progression of IVD degeneration. Studies aimed at elucidating the changing role of TGF-beta signaling in IVD at different pathophysiological stages and its specific molecular mechanisms are needed, and these studies will contribute to safe and effective TGF-beta signaling-based treatments for IVD degeneration. (C) 2019 Osteoarthritis Research Society International. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码：1109 / 1117
页数：9
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