ArticleVirology2011
Osteopontin upregulation in rotavirus-induced murine biliary atresia requires replicating virus but is not necessary for development of biliary atresia.
Article in Virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 13 citations in OpenAlex.
- Gene expression signature for biliary atresia and a role for interleukin-8 in pathogenesis of experimental disease.Hepatology (Baltimore, Md.) · 2014Trial
- Non-Invasive Biomarkers for Assessing Liver Fibrosis in Biliary Atresia: A Literature Review.International journal of molecular sciences · 2026Review
- Identification and validation of oxidative stress-related genes in biliary atresia.Pediatric surgery international · 2025Article
- Rotavirus Infections: Pathophysiology, Symptoms, and Vaccination.Pathogens (Basel, Switzerland) · 2025Review
- Immune-mediated cholangiopathies in children: the need to better understand the pathophysiology for finding the future possible treatment targets.Frontiers in immunology · 2023Review
- Osteopontin Takes Center Stage in Chronic Liver Disease.Hepatology (Baltimore, Md.) · 2021Review
- Low doses of CMV induce autoimmune-mediated and inflammatory responses in bile duct epithelia of regulatory T cell-depleted neonatal mice.Laboratory investigation; a journal of technical methods and pathology · 2015Article
- Article
- Aetiology of biliary atresia: what is actually known?Orphanet journal of rare diseases · 2013Review
- Rotavirus and biliary atresia: can causation be proven?Current opinion in gastroenterology · 2012Review
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 at 1 institution in 1 country.
Funding
Abstract
Biliary atresia (BA) is a progressive fibro-inflammatory pediatric liver disease in which osteopontin (OPN), a glycoprotein with inflammatory and fibrogenic activity, may play a pathogenic role. The current studies were conducted in a mouse model of rotavirus-induced BA to test the hypotheses that live but not inactivated rotavirus causes antigenemia, upregulation of hepatic OPN expression, and induction of BA and fibrosis; and that OPN is necessary for development of BA. Prolonged or transient antigenemia developed in mice inoculated with live or inactivated virus, respectively, but only live virus upregulated hepatic OPN and caused BA and fibrosis. OPN was expressed in intra- and extrahepatic bile ducts in healthy mice and in mice with BA. OPN-deficient mice, similar to WT mice, developed BA. Together, these data show that live but not inactivated rotavirus causes upregulation of hepatic OPN expression and BA but that OPN is not necessary for development of BA.
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.