Evidence map›Paper›PMID 30518128›Full record

ReviewInternational journal of molecular sciences2018

Fibroinflammatory Liver Injuries as Preneoplastic Condition in Cholangiopathies.

Stefania Cannito, Chiara Milani, Andrea Cappon, Maurizio Parola, Mario Strazzabosco, Massimiliano Cadamuro

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 14% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. A Review of CXCL1 in Cardiac Fibrosis.Frontiers in cardiovascular medicine · 2021
    Pooled it
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  13. Notch signalling pathway in development of cholangiocarcinoma.World journal of gastrointestinal oncology · 2020
    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

6 authors at 4 institutions in 2 countries.

Stefania CannitoDepartment of Clinical and Biological Sciences, Unit of Experimental Medicine and Clinical Pathology, University of Torino, Corso Raffaello 30, 10125 Torino, Italy. stefania.cannito@unito.it.ORCID 0000-0001-9883-6882
Chiara MilaniSchool of Medicine and Surgery, University of Milan-Bicocca, Via Cadore 48, 20900 Monza, Italy. chiara.milani@unimib.it.ORCID 0000-0002-3614-9320
Andrea CapponDepartment of Medicine (DIMED), Internal Medicine and Hepatology Unit, University of Padova, Via Giustiniani 2, 35121 Padova, Italy. cappon.andrea@gmail.com.ORCID 0000-0003-0188-2626
Maurizio ParolaDepartment of Clinical and Biological Sciences, Unit of Experimental Medicine and Clinical Pathology, University of Torino, Corso Raffaello 30, 10125 Torino, Italy. mario.strazzabosco@yale.edu.
Mario StrazzaboscoSchool of Medicine and Surgery, University of Milan-Bicocca, Via Cadore 48, 20900 Monza, Italy. mario.strazzabosco@yale.edu.
Massimiliano CadamuroSchool of Medicine and Surgery, University of Milan-Bicocca, Via Cadore 48, 20900 Monza, Italy. massimiliano.cadamuro@gmail.com.ORCID 0000-0002-0899-7613
University of Padua · ITUniversity of Turin · ITUniversity of Milano-Bicocca · ITYale University · US

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
Fondazione Cariplo 2014-1099
6 · The paper itself

Abstract

The cholangipathies are a class of liver diseases that specifically affects the biliary tree. These pathologies may have different etiologies (genetic, autoimmune, viral, or toxic) but all of them are characterized by a stark inflammatory infiltrate, increasing overtime, accompanied by an excess of periportal fibrosis. The cellular types that mount the regenerative/reparative hepatic response to the damage belong to different lineages, including cholagiocytes, mesenchymal and inflammatory cells, which dynamically interact with each other, exchanging different signals acting in autocrine and paracrine fashion. Those messengers may be proinflammatory cytokines and profibrotic chemokines (IL-1, and 6; CXCL1, 10 and 12, or MCP-1), morphogens (Notch, Hedgehog, and WNT/β-catenin signal pathways) and finally growth factors (VEGF, PDGF, and TGFβ, among others). In this review we will focus on the main molecular mechanisms mediating the establishment of a fibroinflammatory liver response that, if perpetuated, can lead not only to organ dysfunction but also to neoplastic transformation. Primary Sclerosing Cholangitis and Congenital Hepatic Fibrosis/Caroli's disease, two chronic cholangiopathies, known to be prodrome of cholangiocarcinoma, for which several murine models are also available, were also used to further dissect the mechanisms of fibroinflammation leading to tumor development.

Indexed as

AnimalsBile Duct DiseasesEpitheliumHumansLiverLiver CirrhosisMesodermPrecancerous ConditionsCaroli’s diseasecholangiocarcinomacholangiocytesneoplastic transformationprimary sclerosing cholangitis

Identifiers

PMID30518128
PMCPMC6321547
OpenAlexW2903061074

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.