Evidence map›Paper›PMID 39250501›Full record

ReviewHepatology (Baltimore, Md.)2025

Central role for cholangiocyte pathobiology in cholestatic liver diseases.

Nidhi Jalan-Sakrikar, Maria Eugenia Guicciardi, Steven P O'Hara, Adiba Azad, Nicholas F LaRusso, Gregory J Gores, Robert C Huebert

Abstract readReview
In one paragraph

Review in Hepatology (Baltimore, Md.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
–field-weighted citation impact
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

31 citing papers in PubMed.

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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.

Nidhi Jalan-SakrikarDepartment of Medicine, Division of Gastroenterology and Hepatology, Mayo College of Medicine and Science, Mayo Clinic, Rochester, Minnesota, USA.ORCID 0000-0001-6795-0121
Maria Eugenia GuicciardiDepartment of Medicine, Division of Gastroenterology and Hepatology, Mayo College of Medicine and Science, Mayo Clinic, Rochester, Minnesota, USA.
Steven P O'HaraDepartment of Medicine, Division of Gastroenterology and Hepatology, Mayo College of Medicine and Science, Mayo Clinic, Rochester, Minnesota, USA.
Adiba AzadDepartment of Medicine, Division of Gastroenterology and Hepatology, Mayo College of Medicine and Science, Mayo Clinic, Rochester, Minnesota, USA.
Nicholas F LaRussoDepartment of Medicine, Division of Gastroenterology and Hepatology, Mayo College of Medicine and Science, Mayo Clinic, Rochester, Minnesota, USA.
Gregory J GoresDepartment of Medicine, Division of Gastroenterology and Hepatology, Mayo College of Medicine and Science, Mayo Clinic, Rochester, Minnesota, USA.
Robert C HuebertDepartment of Medicine, Division of Gastroenterology and Hepatology, Mayo College of Medicine and Science, Mayo Clinic, Rochester, Minnesota, USA.ORCID 0000-0002-9812-7573

Funding

PILOT AND FEASIBILTY PROGRAMP30DK084567 · NIDDK · MAYO CLINIC ROCHESTER · PI GREGORY J. GORES · 2009 to 2026
$22.2M
Institutional Career Development CoreKL2TR002379 · NCATS · MAYO CLINIC ROCHESTER · PI NILUFER ERTEKIN-TANER · 2017 to 2026
$14.9M
The Pathobiology of Hepatic EpitheliaR01DK024031 · NIDDK · MAYO CLINIC ROCHESTER · PI LARUSSO, NICHOLAS F. · 1986 to 2023
$10.4M
Pathophysiology of Biliary DiseaseR01DK057993 · NIDDK · MAYO CLINIC ROCHESTER · PI LARUSSO, NICHOLAS F., O'HARA, STEVEN P · 2001 to 2025
$7.1M
Molecular Mechanisms of Cholestatic FibrogenesisR01DK117861 · NIDDK · MAYO CLINIC ROCHESTER · PI Robert Christian Huebert · 2019 to 2026
$2.8M
Cholestatic Liver InjuryR01DK124182 · NIDDK · MAYO CLINIC ROCHESTER · PI GORES, GREGORY J. · 2020 to 2023
$1.4M
NCATS NIH HHS KL2 TR002379NIDDK NIH HHS P30 DK084567NIDDK NIH HHS R01 DK024031NIDDK NIH HHS R01 DK057993NIDDK NIH HHS R01 DK117861NIDDK NIH HHS R01 DK124182
6 · The paper itself

Abstract

Cholangiopathies comprise a spectrum of chronic intrahepatic and extrahepatic biliary tract disorders culminating in progressive cholestatic liver injury, fibrosis, and often cirrhosis and its sequela. Treatment for these diseases is limited, and collectively, they are one of the therapeutic "black boxes" in clinical hepatology. The etiopathogenesis of the cholangiopathies likely includes disease-specific mediators but also common cellular and molecular events driving disease progression (eg, cholestatic fibrogenesis, inflammation, and duct damage). The common pathways involve cholangiocytes, the epithelial cells lining the intrahepatic and extrahepatic bile ducts, which are central to the pathogenesis of these disorders. Current information suggests that cholangiocytes function as a signaling "hub" in biliary tract-associated injury. Herein, we review the pivotal role of cholangiocytes in cholestatic fibrogenesis, focusing on the crosstalk between cholangiocytes and portal fibroblasts and HSCs. The proclivity of these cells to undergo a senescence-associated secretory phenotype, which is proinflammatory and profibrogenic, and the intrinsic intracellular activation pathways resulting in the secretion of cytokines and chemokines are reviewed. The crosstalk between cholangiocytes and cells of the innate (neutrophils and macrophages) and adaptive (T cells and B cells) immune systems is also examined in detail. The information will help consolidate information on this topic and guide further research and potential therapeutic strategies for these diseases.

Indexed as

Bile DuctsCholestasisEpithelial CellsAnimalsHumansbiliary atresiaductular reactionPBC (primary biliary cholangitis)PSC (primary sclerosing cholangitis)senescence

Identifiers

PMID39250501
PMCPMC11890218

What OpenQuestion holds

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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.