ArticleBMC pediatrics2025
Immune and genetic landscapes of biliary atresia: a pathway to precision medicine.
Article in BMC pediatrics, 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.
- Liver fibrosis in biliary atresia: identification of the key gene EDIL3 via integrated bioinformatics.Frontiers in medicine · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBiliary atresia (BA) is a rare pediatric cholestatic disorder characterized by progressive bile duct inflammation and fibrosis. The underlying molecular mechanisms of BA remain poorly defined. This study aimed to identify susceptibility genes causally associated with BA by integrating genome-wide association study (GWAS) and transcriptomic data, and to explore their potential immunopathological roles.
methodsTwo independent BA transcriptomic datasets from the Gene Expression Omnibus (GEO) were analyzed, and Mendelian randomization (MR) was applied to assess causal associations between differentially expressed genes (DEGs) and BA. Co-expressed genes were further evaluated for biological pathway enrichment and immune cell infiltration patterns. Expression levels of candidate genes were validated using quantitative real-time PCR (qRT-PCR) in liver tissues from 20 BA patients and 10 normal controls. Representative liver histopathology was also examined.
resultsWe identified 816 DEGs, including 458 upregulated and 358 downregulated genes. MR analysis highlighted seven co-expressed genes with potential causal relevance to BA, including C12orf75, PSD3, CRIM1, CHIT1 (upregulated), and SEC14L4, MAPRE3, TCEA3 (downregulated). qRT-PCR validation confirmed significantly elevated expression of C12orf75, PSD3, and CHIT1, and reduced expression of TCEA3 in BA liver tissues compared to controls (P < 0.05), consistent with MR predictions. Histopathological analysis revealed severe portal fibrosis, bile duct proliferation, and pseudolobule formation in BA samples, whereas normal controls exhibited preserved hepatic architecture with minimal fibrotic changes.
conclusionThis study identifies a panel of immune- and transcription-related genes with potential causal roles in BA and validates their expression in human liver tissue. These findings offer new insights into the genetic and molecular basis of BA, supporting future efforts in subtype classification and immunomodulatory therapeutic development.
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.