Tumor necrosis factor-α: a key contributor to intervertebral disc degeneration.

Abstract

Intervertebral disc (IVD) degeneration (IDD) is the most common cause leading to low back pain (LBP), which is a highly prevalent, costly, and crippling condition worldwide. Current treatments for IDD are limited to treat the symptoms and do not target the pathophysiology. Tumor necrosis factor-α (TNF-α) is one of the most potent pro-inflammatory cytokines and signals through its receptors TNFR1 and TNFR2. TNF-α is highly expressed in degenerative IVD tissues, and it is deeply involved in multiple pathological processes of disc degeneration, including matrix destruction, inflammatory responses, apoptosis, autophagy, and cell proliferation. Importantly, anti-TNF-α therapy has shown promise for mitigating disc degeneration and relieving LBP. In this review, following a brief description of TNF-α signal transduction, we mainly focus on the expression pattern and roles of TNF-α in IDD, and summarize the emerging progress regarding its inhibition as a promising biological therapeutic approach to disc degeneration and associated LBP. A better understanding will help to develop novel TNF-α-centered therapeutic interventions for degenerative disc disease.

• Authors: Cheng Wang, Xiaohua Yu, Yiguo Yan, Wei Yang, Shujun Zhang, Yongxiao Xiang, Jian Zhang, Wenjun Wang
• Journal: Acta biochimica et biophysica Sinica (Acta Biochim Biophys Sin (Shanghai)) Vol. 49 Issue 1 Pg. 1-13 (Jan 2017) ISSN: 1745-7270 [Electronic] China
• PMID: 27864283 (Publication Type: Journal Article, Review)
• Copyright: © The Author 2016. Published by Oxford University Press on behalf of the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences. All rights reserved. For permissions, please e-mail: [email protected].

Chemical References

• Tumor Necrosis Factor-alpha

Topics

• Humans
• Intervertebral Disc Degeneration (physiopathology)
• Protein Conformation
• Signal Transduction
• Tumor Necrosis Factor-alpha (chemistry, physiology)