SynthesisArthritis & rheumatology (Hoboken, N.J.)2025
Cross-Phenotype Genome-Wide Association Study on the Shared Genetic Susceptibility to Systemic Sclerosis and Primary Biliary Cholangitis.
Synthesis in Arthritis & rheumatology (Hoboken, N.J.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Novel pleiotropic loci link vascular and immune pathways in systemic sclerosis and primary Raynaud's phenomenon.Rheumatology (Oxford, England) · 2026Pooled it
- Shared Genetic Architecture of Premenstrual Disorder and Postpartum Depression: Registry-Based and Genetic Evidence.Research square · 2026Article
- Multilevel Exploration of Shared Genetic Architecture Between Primary Biliary Cholangitis and Four Autoimmune Diseases.Endocrine, metabolic & immune disorders drug targets · 2026Article
- Autoimmune liver diseases and systemic rheumatic disorders: exploring their interplay and impact on prognosis.BMC gastroenterology · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
objectiveAn increased risk of primary biliary cholangitis (PBC) has been reported in patients with systemic sclerosis (SSc). Our study aims to investigate the shared genetic susceptibility between the two disorders and to define candidate causal genes using cross-phenotype genome-wide association study (GWAS) meta-analysis.
methodsWe performed cross-phenotype GWAS meta-analysis and Bayesian colocalization analysis for patients with SSc and patients with PBC. We performed both genome-wide and locus-based analysis, including tissue and pathway enrichment analyses, fine-mapping, Bayesian colocalization analyses with expression quantitative trait loci and protein quantitative trait loci (pQTL) datasets, and phenome-wide association studies. Finally, we used an integrative approach to prioritize candidate causal genes from the novel loci.
resultsWe detected a strong genetic correlation between SSc and PBC (global genetic correlation = 0.84, P = 1.7 × 10
conclusionOur study supports a strong shared genetic susceptibility between SSc and PBC. Using cross-phenotype analyses, we have prioritized several novel candidate causal genes and pathways for these disorders.
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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 Socratic graph.