IL-37 alleviates intervertebral disc degeneration via the IL-1R8/NF-κB pathway

Li, Sunlong; Pan, Xiangxiang; Wu, Yuhao; Tu, Yiting; Hong, Weijun; Ren, Jiaping; Miao, Jiansen; Wang, Tengjie; Xia, Weiyi; Lu, Jiajie; Chen, Jiaoxiang; Hu, Xianluo; Zhang, Xiaolei; Wang, Xiangyang

doi:10.1016/j.joca.2023.01.006

Cited by 11 publications

(5 citation statements)

References 46 publications

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“…LBP is mainly correlated with intervertebral disk degeneration-related diseases 5 . To explore the biological effects of different mRNAs in degenerative discs, we analyzed the microarray data (GSE70362) of 3 degenerative tissue samples versus 3 nondegenerative tissue samples.…”

Section: Resultsmentioning

confidence: 99%

“…The H type vessels played an important role in bone metabolism balance. We performed immunofluorescence staining and the results showed that, compared with the sham group, the LSI mice had more CD31 hi Emcn hi cells in the endplate area at 2, 4 and 8 weeks after LSI operation (Fig 3G) LBP is mainly correlated with intervertebral disk degeneration-related diseases 5 . To explore the biological effects of different mRNAs in degenerative discs, we analyzed the microarray data (GSE70362) of 3 degenerative tissue samples versus 3 nondegenerative (which was not certified by peer review) is the author/funder.…”

Section: Introductionmentioning

confidence: 95%

“…LBP is mainly correlated with intervertebral disk degeneration and endplate injury 5,6 . In clinical, LBP caused by endplate injuries is quite common.…”

Section: Introductionmentioning

confidence: 99%

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Targeting GDF15 as a potential therapy for low back pain originating from endplate

Kong

et al. 2023

Preprint

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The overactivation of osteoclasts in the endplate is one of the most important causes of low back pain (LBP) originating from endplate. Transforming growth factor-β family has been demonstrated to play an important role during osteoclast differentiation. GDF15 was reported to participate in several pathological states. In this study, we reported that the lumbar spine instability (LSI) induced the overactivation of osteoclasts and CD31hiEmcnhi endothelial vessels in the bony endplate. In addition, the expression of GDF15 in human disc samples and mice models were also increased. GDF15 could promote the fusion of preosteoclasts via Rac1/Cdc42/PAK/Cofilin axis, and facilitate the angiogenesis via the secretion of PDGF-BB. Furthermore, we proved that the GDF15 inhibitor, CTL-002 could reduce the expression of GDF15 in the endplate and alleviate the overactivation of osteoclasts and CD31hiEmcnhi endothelial vessels induced by LSI in vivo. In conclusion, we demonstrated that GDF15 could regulates the fusion of preosteoclasts and targeting GDF15 in the endplate served as a novel anabolic therapy for low back pain treatment.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 95%

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Targeting GDF15 as a potential therapy for low back pain originating from endplate

Kong

et al. 2023

Preprint

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“…Certain CIPs can cause IVD cells to senescence and apoptosis, activate proteolytic enzymes to increase extracellular matrix (ECM) degradation, and aid in the infiltration of immune cells to amplify the inflammatory response, all of which can lead to the formation of SDDs 11 . However, by suppressing senescence and SASP production, downregulating pro‐inflammatory cytokines and chemokines to avoid inflammation, and encouraging repair and regeneration through the deposition of IVD‐important proteins, other CIPs can postpone the development of IVDD 12,13 . Reports on the association between CIPs and the onset of SDDs are controversial, and bias due to the combination of confounding factors, environmental factors, and reverse causation is one of the main reasons why these studies are contradictory.…”

Section: Introductionmentioning

confidence: 99%

“… 11 However, by suppressing senescence and SASP production, downregulating pro‐inflammatory cytokines and chemokines to avoid inflammation, and encouraging repair and regeneration through the deposition of IVD‐important proteins, other CIPs can postpone the development of IVDD. 12 , 13 Reports on the association between CIPs and the onset of SDDs are controversial, and bias due to the combination of confounding factors, environmental factors, and reverse causation is one of the main reasons why these studies are contradictory. A great deal of work has been done on the interconnections between CIPs and the multiple pathogenic mechanisms of SDDs.…”

Section: Introductionmentioning

confidence: 99%

Effects of circulating inflammatory proteins on spinal degenerative diseases: Evidence from genetic correlations and Mendelian randomization study

Zheng,

Lin,

Wang

et al. 2024

JOR Spine

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BackgroundNumerous investigations have suggested links between circulating inflammatory proteins (CIPs) and spinal degenerative diseases (SDDs), but causality has not been proven. This study used Mendelian randomization (MR) to investigate the causal associations between 91 CIPs and cervical spondylosis (CS), prolapsed disc/slipped disc (PD/SD), spinal canal stenosis (SCS), and spondylolisthesis/spondylolysis.MethodsGenetic variants data for CIPs and SDDs were obtained from the genome‐wide association studies (GWAS) database. We used inverse variance weighted (IVW) as the primary method, analyzing the validity and robustness of the results through pleiotropy and heterogeneity tests and performing reverse MR analysis to test for reverse causality.ResultsThe IVW results with Bonferroni correction indicated that beta‐nerve growth factor (β‐NGF), C‐X‐C motif chemokine 6 (CXCL6), and interleukin‐6 (IL‐6) can increase the risk of CS. Fibroblast growth factor 19 (FGF19), sulfotransferase 1A1 (SULT1A1), and tumor necrosis factor‐beta (TNF‐β) can increase PD/SD risk, whereas urokinase‐type plasminogen activator (u‐PA) can decrease the risk of PD/SD. FGF19 and TNF can increase SCS risk. STAM binding protein (STAMBP) and T‐cell surface glycoprotein CD6 isoform (CD6 isoform) can increase the risk of spondylolisthesis/spondylolysis, whereas monocyte chemoattractant protein 2 (MCP2) and latency‐associated peptide transforming growth factor beta 1 (LAP‐TGF‐β1) can decrease spondylolisthesis/spondylolysis risk.ConclusionsMR analysis indicated the causal associations between multiple genetically predicted CIPs and the risk of four SDDs (CS, PD/SD, SCS, and spondylolisthesis/spondylolysis). This study provides reliable genetic evidence for in‐depth exploration of the involvement of CIPs in the pathogenic mechanism of SDDs and provides novel potential targets for SDDs.

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FSTL1 Accelerates Nucleus Pulposus Cell Senescence and Intervertebral Disc Degeneration Through TLR4/NF-κB Pathway

Yan,

Ding,

Zhang

et al. 2024

Inflammation

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IL-37 alleviates intervertebral disc degeneration via the IL-1R8/NF-κB pathway

Cited by 11 publications

References 46 publications

Targeting GDF15 as a potential therapy for low back pain originating from endplate

Targeting GDF15 as a potential therapy for low back pain originating from endplate

Effects of circulating inflammatory proteins on spinal degenerative diseases: Evidence from genetic correlations and Mendelian randomization study

FSTL1 Accelerates Nucleus Pulposus Cell Senescence and Intervertebral Disc Degeneration Through TLR4/NF-κB Pathway

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