Evidence map›Paper›PMID 26008129›Full record

ReviewNature reviews. Gastroenterology & hepatology2015

Pathogenesis of biliary atresia: defining biology to understand clinical phenotypes.

Akihiro Asai, Alexander Miethke, Jorge A Bezerra

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Gastroenterology & hepatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 149 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
149citing papers in PubMed, 2 pooled it
13.3field-weighted citation impact, top 1% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

149 citing papers in PubMed, 2 syntheses or guidelines pooled it, 275 citations in OpenAlex.

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89 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Akihiro AsaiDivision of Pediatric Gastroenterology, Hepatology, and Nutrition, Department of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati, 3333 Burnet Avenue, Cincinnati, OH 45229-3039, USA.
Alexander MiethkeDivision of Pediatric Gastroenterology, Hepatology, and Nutrition, Department of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati, 3333 Burnet Avenue, Cincinnati, OH 45229-3039, USA.
Jorge A BezerraDivision of Pediatric Gastroenterology, Hepatology, and Nutrition, Department of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati, 3333 Burnet Avenue, Cincinnati, OH 45229-3039, USA.
Cincinnati Children's Hospital Medical Center · US

Funding

Stem Cell/Organoid and Genome Editing CoreP30DK078392 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI Alexander Miethke · 2007 to 2026
$24.4M
Clinical Center for Cholestatic Liver Disease in ChildrenU01DK062497 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI Alexander Miethke · 2002 to 2026
$13.2M
Immunologic Dysfunction in Biliary AtresiaR01DK064008 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI DENSON, LEE ARMISTEAD · 2003 to 2022
$6.7M
Biological Basis of Phenotypes and Clinical Outcomes in Biliary AtresiaR01DK083781 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI BEZERRA, JORGE A. · 2009 to 2023
$6.1M
The role of regulatory T cells in biliary atresiaR01DK095001 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI Alexander Miethke · 2012 to 2026
$4.4M
NIDDK NIH HHS DK62497NIDDK NIH HHS DK64008NIDDK NIH HHS DK83781NIDDK NIH HHS DK95001NIDDK NIH HHS P30 DK078392NIDDK NIH HHS R01 DK064008NIDDK NIH HHS R01 DK083781NIDDK NIH HHS R01 DK095001NIDDK NIH HHS U01 DK062497
6 · The paper itself

Abstract

Biliary atresia is a severe cholangiopathy of early infancy that destroys extrahepatic bile ducts and disrupts bile flow. With a poorly defined disease pathogenesis, treatment consists of the surgical removal of duct remnants followed by hepatoportoenterostomy. Although this approach can improve the short-term outcome, the liver disease progresses to end-stage cirrhosis in most children. Further improvement in outcome will require a greater understanding of the mechanisms of biliary injury and fibrosis. Here, we review progress in the field, which has been fuelled by collaborative studies in larger patient cohorts and the development of cell culture and animal model systems to directly test hypotheses. Advances include the identification of phenotypic subgroups and stages of disease based on clinical, pathological and molecular features. Stronger evidence exists for viruses, toxins and gene sequence variations in the aetiology of biliary atresia, triggering a proinflammatory response that injures the duct epithelium and produces a rapidly progressive cholangiopathy. The immune response also activates the expression of type 2 cytokines that promote epithelial cell proliferation and extracellular matrix production by nonparenchymal cells. These advances provide insight into phenotype variability and might be relevant to the design of personalized trials to block progression of liver disease.

Indexed as

Biliary AtresiaAnimalsCell ProliferationCytokinesDisease Models, AnimalHumansInfantInfant, NewbornCytokines

Identifiers

PMID26008129
PMCPMC4877133
OpenAlexW1945197404

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.