Evidence map›Paper›PMID 26610202›Full record

ArticleHepatology (Baltimore, Md.)2016

Cholestasis-induced adaptive remodeling of interlobular bile ducts.

Nachiket Vartak, Amruta Damle-Vartak, Beate Richter, Olaf Dirsch, Uta Dahmen, Seddik Hammad, Jan G Hengstler

Open access · hybridAbstract read
In one paragraph

Article in Hepatology (Baltimore, Md.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
6.8field-weighted citation impact, top 2% 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

55 citing papers in PubMed, 116 citations in OpenAlex.

  1. The Role of Gut Microbiota in Liver Regeneration After Partial Hepatectomy: New Evidence From Animal and Human Studies.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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  9. A modular analysis of bile canalicular function and its implications for cholestasis.American journal of physiology. Gastrointestinal and liver physiology · 2023
    Review
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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

7 authors at 4 institutions in 2 countries.

Nachiket VartakDepartment of Systems Toxicology, Leibniz Institute for Work Physiology and Human Factors (IfADo) at TU Dortmund, Dortmund, Germany.
Amruta Damle-VartakDepartment of Systems Toxicology, Leibniz Institute for Work Physiology and Human Factors (IfADo) at TU Dortmund, Dortmund, Germany.
Beate RichterDepartment of Experimental Transplantation Surgery, University Clinic Jena, Jena, Germany.
Olaf DirschDepartment of Experimental Transplantation Surgery, University Clinic Jena, Jena, Germany.
Uta DahmenDepartment of Experimental Transplantation Surgery, University Clinic Jena, Jena, Germany.
Seddik HammadDepartment of Systems Toxicology, Leibniz Institute for Work Physiology and Human Factors (IfADo) at TU Dortmund, Dortmund, Germany.
Jan G HengstlerDepartment of Systems Toxicology, Leibniz Institute for Work Physiology and Human Factors (IfADo) at TU Dortmund, Dortmund, Germany.
Jena University Hospital · DELeibniz Research Centre for Working Environment and Human Factors · DESouth Valley University · EGTU Dortmund University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

unlabelledCholestasis is a common complication in liver diseases that triggers a proliferative response of the biliary tree. Bile duct ligation (BDL) is a frequently used model of cholestasis in rodents. To determine which changes occur in the three-dimensional (3D) architecture of the interlobular bile duct during cholestasis, we used 3D confocal imaging, surface reconstructions, and automated image quantification covering a period up to 28 days after BDL. We show a highly reproducible sequence of interlobular duct remodeling, where cholangiocyte proliferation initially causes corrugation of the luminal duct surface, leading to an approximately five-fold increase in surface area. This is analogous to the function of villi in the intestine or sulci in the brain, where an expansion of area is achieved within a restricted volume. The increase in surface area is further enhanced by duct branching, branch elongation, and loop formation through self-joining, whereby an initially relatively sparse mesh surrounding the portal vein becomes five-fold denser through elongation, corrugation, and ramification. The number of connections between the bile duct and the lobular bile canalicular network by the canals of Hering decreases proportionally to the increase in bile duct length, suggesting that no novel connections are established. The diameter of the interlobular bile duct remains constant after BDL, a response that is qualitatively distinct from that of large bile ducts, which tend to enlarge their diameters. Therefore, volume enhancement is only due to net elongation of the ducts. Because curvature and tortuosity of the bile duct are unaltered, this enlargement of the biliary tree is caused by branching and not by convolution.

conclusionBDL causes adaptive remodeling that aims at optimizing the intraluminal surface area by way of corrugation and branching.

Indexed as

AnimalsBile DuctsCholestasisDisease Models, AnimalLigationMice, Inbred C57BL

Identifiers

PMID26610202
PMCPMC5066759
OpenAlexW2295539298

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.