ArticleJOR spine2024
Effects of circulating inflammatory proteins on spinal degenerative diseases: Evidence from genetic correlations and Mendelian randomization study.
Article in JOR spine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed.
- The safety, tolerability, pharmacokinetics, and pharmacodynamics of nebulized pegylated interferon α-2b in healthy adults: a randomized phase 1 trial.BMC pharmacology & toxicology · 2025Trial
- Identification of immune-mediated aging genes associated with cervical spondylosis through single-cell eQTL Mendelian randomization.Frontiers in immunology · 2026Article
- Mendelian Randomization Research Examining the Effects of Insomnia on Herpes Zoster and Postherpetic Neuralgia.Pain research & management · 2026Article
- Causal correlation between inflammatory cytokines and hypertrophic scar based on two-sample Mendelian randomization.Journal, genetic engineering & biotechnology · 2025Article
- Degenerative Lumbosacral Spinal Stenosis Alters Neurotrophin-3 and -4 Expression: Impact of Metabolic and Behavioral Factors.Current issues in molecular biology · 2025Article
- Immune-mediated bone loss: A Mendelian randomization and NHANES-based study of viral infections and osteoporosis.Virus research · 2025Article
- Article
- Causal relationship between gut microbiota and viral infectious disease: A 2-sample Mendelian randomization study.Medicine · 2025Article
- Article
- The causal relationship between circulating inflammatory proteins and heart failure: A two-sample Mendelian randomization study.Medicine · 2025Article
- No Evidence for a Causal Association Between Depression and Herpes Zoster or Post-Herpetic Neuralgia: A Mendelian Randomization Study.Journal of pain research · 2025Article
- Novel therapeutic targets for metabolism-related diseases: proteomic Mendelian randomization and colocalization analyses.Therapeutic advances in endocrinology and metabolism · 2025Article
- Article
- Causal association between circulating inflammatory proteins and peripheral artery disease: a bidirectional two-sample Mendelian randomization study.Frontiers in immunology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Numerous 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. Methods: Genetic 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. Results: The 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. Conclusions: MR 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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.