ArticleFrontiers in physiology2020
Systems Analysis of Biliary Atresia Through Integration of High-Throughput Biological Data.
Article in Frontiers in physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Article
- Transcriptional analysis of murine biliary atresia identifies macrophage heterogeneity and subset-specific macrophage functions.Frontiers in immunology · 2025Article
- Molecular Mechanisms of Fibrosis in Cholestatic Liver Diseases and Regenerative Medicine-Based Therapies.Cells · 2024Review
- Biliary atresia.Nature reviews. Disease primers · 2024Review
- Biliary atresia is associated with polygenic susceptibility in ciliogenesis and planar polarity effector genes.Journal of hepatology · 2023Article
- Structural and Functional Modulation of Gut Microbiota by Jiangzhi Granules during the Amelioration of Nonalcoholic Fatty Liver Disease.Oxidative medicine and cellular longevity · 2021Article
Corrections and comments
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Authors and funding
6 authors at 5 institutions in 1 country.
Funding
Abstract
Biliary atresia (BA), blockage of the proper bile flow due to loss of extrahepatic bile ducts, is a rare, complex disease of the liver and the bile ducts with unknown etiology. Despite ongoing investigations to understand its complex pathogenesis, BA remains the most common cause of liver failure requiring liver transplantation in children. To elucidate underlying mechanisms, we analyzed the different types of high-throughput genomic and transcriptomic data collected from the blood and liver tissue samples of children suffering from BA. Through use of a novel integrative approach, we identified potential biomarkers and over-represented biological functions and pathways to derive a comprehensive network showing the dysfunctional mechanisms associated with BA. One of the pathways highlighted in the integrative network was hypoxia signaling. Perturbation with hypoxia inducible factor activator, dimethyloxalylglycine, induced the biliary defects of BA in a zebrafish model, serving as a validation for our studies. Our approach enables a systems-level understanding of human BA biology that is highlighted by the interaction between key biological functions such as fibrosis, inflammation, immunity, hypoxia, and development.
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Registered trials
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