Interleukin-1β in intervertebral disk degeneration

Yang, Wei; Yu, Xiaohua; Wang, Cheng; He, Wen-Si; Zhang, Shujun; Yan, Yongping; Zhang, Jian; Xiang, Yong‐Xiao; Wang, Wenjun

doi:10.1016/j.cca.2015.08.029

Cited by 113 publications

(82 citation statements)

References 131 publications

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“…MMPs and ADAMTSs are primary enzymes that are responsible for ECM degradation. Tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), both major pro-inflammatory cytokines, are highly expressed in degenerated IVD cells and tissues, and have been shown to increase the levels of MMPs and ADAMTSs [89,90]. In rat NP cells exposed to TNF-α or IL-1β, the expression of autophagy-related genes does not change; however, rapamycin (an autophagy activator) decreases the levels of MMP-3, MMP-9 and ADAMTS-4, and an opposite effect appears when treated with 3-MA (an autophagy inhibitor) [91].…”

Section: Autophagy Protects Against Disc Degenerationmentioning

confidence: 99%

Autophagy: A double-edged sword in intervertebral disk degeneration

Zhang

Yang

Wang

et al. 2016

Clinica Chimica Acta

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Section: Autophagy Protects Against Disc Degenerationmentioning

confidence: 99%

Autophagy: A double-edged sword in intervertebral disk degeneration

Zhang

Yang

Wang

et al. 2016

Clinica Chimica Acta

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“…As the second most common cause of doctor visits, LBP has become a major factor affecting quality of life and leads to an enormous socioeconomic burden. There are many causes in the etiology of LBP, among which intervertebral disc (IVD) herniation and IVD degeneration (IDD) are the most common diagnoses and targets for intervention [2]. IDD is a multifactorial process characterized by cellular and biochemical changes in disc tissues that lead to structural failure, and it is currently attributed to the interaction between environmental and genetic factors (Fig.…”

Section: Introductionmentioning

confidence: 99%

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

Wang¹,

Yu²,

Yan³

et al. 2017

ABBS

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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.

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“…Apart from MMPs and ADAMTSs, cytokines can also promote the chemokine ligand (CCL) expression in intervertebral disc cells. In terms of previous studies, CCLs can induce macrophage migration into the IVD, deteriorating the inflammatory stage and causing pain (12–17). …”

Section: Introductionmentioning

confidence: 78%

Carthamin yellow inhibits matrix degradation and inflammation induced by LPS in the intervertebral disc via suppression of MAPK pathway activation

Chen

Wang

et al. 2017

Experimental and Therapeutic Medicine

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Carthamin yellow (CY), which is a flavonoid compound isolated from safflower, has various pharmacological effects including promoting blood circulation to remove blood stasis and alleviating pain. CY is a herb used in Chinese traditional medicines. Intervertebral disc degeneration (IDD) is a common spinal disorder and degeneration of nucleus pulposus (NP) cells and inflammation are significant parts of the pathological cascade. The curative effect of CY on NP cells in association with degeneration and inflammation remains to be elucidated. In the present study, rat NP cells were isolated, cultured and used to detect the suppressive effects of CY on lipopolysaccharide (LPS)-induced genetic expression variation and the expression of matrix degradation enzymes, including matrix metallopeptidase-3, ADAM metallopeptidase with thrombospondin type 1 motif (ADAMTS)-4 and ADAMTS-5. A protective effect of CY on NP cells was observed against LPS-induced matrix degradation and inflammation. Western blotting results demonstrated that pretreatment with CY significantly suppressed the LPS-induced activation of the mitogen activated protein kinase (MAPK) pathway. The results of the present study suggested that CY exerted anti-degenerative and anti-inflammatory effects on NP cells via inhibition of MAPK pathway activation. Therefore, CY may be a potential therapeutic drug for the treatment of IDD in the future.

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Interleukin-1β in intervertebral disk degeneration

Cited by 113 publications

References 131 publications

Autophagy: A double-edged sword in intervertebral disk degeneration

Autophagy: A double-edged sword in intervertebral disk degeneration

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

Carthamin yellow inhibits matrix degradation and inflammation induced by LPS in the intervertebral disc via suppression of MAPK pathway activation

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Interleukin-1β in intervertebral disk degeneration

Cited by 113 publications

References 131 publications

Autophagy: A double-edged sword in intervertebral disk degeneration

Autophagy: A double-edged sword in intervertebral disk degeneration

Tumor necrosis factor-&alpha;: a key contributor to intervertebral disc degeneration

Carthamin yellow inhibits matrix degradation and inflammation induced by LPS in the intervertebral disc via suppression of MAPK pathway activation

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