ArticleJournal of molecular neuroscience : MN2025
Genetic Association of CANT1 Gene with Scoliosis: An Integrative Study Involving Methylation, Immune Factors, and Metabolites.
Article in Journal of molecular neuroscience : MN, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Dysregulation of the Cant1/β-Catenin/TCF4-CHSY1 Axis Underpins Impaired ECM Biosynthesis in Skeletal Disorders.Research (Washington, D.C.) · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
The CANT1 gene, encoding a nucleotidase linked to calcium signaling, is crucial for spinal development, with its deficiency causing skeletal developmental issues. However, the relationship between CANT1 and scoliosis remains unclear. This study aims to explore the role of CANT1 in scoliosis from a genetic perspective and its potential as a therapeutic target. This study employed a multi-method approach, including Mendelian Randomization (MR) analysis, colocalization analysis, mediation analysis, enrichment analysis, PPI network construction, and molecular docking. Using eQTL and pQTL databases, the Inverse Variance Weighted (IVW) method identified key genes associated with scoliosis. Colocalization analysis pinpointed genes with strong causal links to scoliosis. Mediation analysis assessed the impact of CANT1 methylation, immune cells, inflammatory factors, and plasma metabolites on scoliosis. Enrichment analysis identified biological pathways enriched in scoliosis-related genes. The PPI network was constructed using the STRING database, and CANT1 expression in bone marrow and skeletal muscle was analyzed via the Human Protein Atlas. Potential therapeutic compounds were identified through the DSigDB database and validated by molecular docking. We identified 94 key genes associated with scoliosis, primarily involved in purine ribonucleotide metabolism. Colocalization analysis provided strong evidence linking CANT1 to scoliosis. Further analysis revealed that methylation sites, immune cells, inflammatory factors, and plasma metabolites related to CANT1 may play roles in scoliosis pathogenesis. The regulatory expression of CANT1 was examined using the STRING database and the Human Protein Atlas. Six candidate compounds with favorable binding affinity to CANT1 were identified through DSigDB and molecular docking. This study offers new insights into the pathogenesis of scoliosis and highlights CANT1 as a potential therapeutic target. CANT1 may influence scoliosis development through multiple pathways, including methylation, immune cells, inflammatory factors, and plasma metabolites. Further experimental validation is needed to confirm these findings and explore the therapeutic potential of the identified compounds.
Indexed as
Identifiers
40775174What 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.