Affiliation:
1. Department of Spinal Surgery The First Affiliated Hospital of Fujian Medical University Fuzhou China
2. Department of Orthopedic Surgery Fujian Medical University Union Hospital Fuzhou China
3. Arthritis Clinical and Research Center, Peking University People's Hospital Beijing China
4. Department of Microbiology, Immunology and Infectious Diseases University of Calgary Calgary Alberta Canada
Abstract
AbstractBackgroundNumerous 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.
Funder
Natural Science Foundation of Fujian Province
Fujian Provincial Health Technology Project
National Natural Science Foundation of China
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