Evidence map›Paper›PMID 25681399›Full record

ReviewGut2015

Pathobiology of liver fibrosis: a translational success story.

Youngmin A Lee, Michael C Wallace, Scott L Friedman

Erratum issuedAbstract readReview
In one paragraph

Review in Gut, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 469 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
469citing papers in PubMed, 7 pooled it
46.0field-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

469 citing papers in PubMed, 7 syntheses or guidelines pooled it, 895 citations in OpenAlex.

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  8. Article
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  10. Review
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  12. Hepatic stellate cells in alcoholic liver cirrhosis: mechanisms of fibrogenesis, plasticity, and fibrosis reversal.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026
    Review
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409 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Youngmin A LeeDivision of Liver Diseases, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Michael C WallaceDivision of Liver Diseases, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Scott L FriedmanDivision of Liver Diseases, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Icahn School of Medicine at Mount Sinai · US

Funding

The Role of KLF6 in Hepatic FibrosisR01DK056621 · NIDDK · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI FRIEDMAN, SCOTT L. · 2000 to 2019
$6.2M
Autophagy during hepatic stellate cell activation in alcoholic liver injuryR01AA020709 · NIAAA · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI FRIEDMAN, SCOTT L. · 2011 to 2015
$1.8M
NIAAA NIH HHS R01 AA020709NIAAA NIH HHS R01AA020709NIDDK NIH HHS R01 DK056621NIDDK NIH HHS R01DK56621
6 · The paper itself

Abstract

Reversibility of hepatic fibrosis and cirrhosis following antiviral therapy for hepatitis B or C has advanced the prospect of developing antifibrotic therapies for patients with chronic liver diseases, especially non-alcoholic steatohepatitis. Mechanisms of fibrosis have focused on hepatic stellate cells, which become fibrogenic myofibroblasts during injury through 'activation', and are at the nexus of efforts to define novel drug targets. Recent studies have clarified pathways of stellate cell gene regulation and epigenetics, emerging pathways of fibrosis regression through the recruitment and amplification of fibrolytic macrophages, nuanced responses of discrete inflammatory cell subsets and the identification of the 'ductular reaction' as a marker of severe injury and repair. Based on our expanded knowledge of fibrosis pathogenesis, attention is now directed towards strategies for antifibrotic therapies and regulatory challenges for conducting clinical trials with these agents. New therapies are attempting to: 1) Control or cure the primary disease or reduce tissue injury; 2) Target receptor-ligand interactions and intracellular signaling; 3) Inhibit fibrogenesis; and 4) Promote resolution of fibrosis. Progress is urgently needed in validating non-invasive markers of fibrosis progression and regression that can supplant biopsy and shorten the duration of clinical trials. Both scientific and clinical challenges remain, however the past three decades of steady progress in understanding liver fibrosis have contributed to an emerging translational success story, with realistic hopes for antifibrotic therapies to treat patients with chronic liver disease in the near future.

Indexed as

Clinical Trials as TopicDrug DiscoveryHepatic Stellate CellsHumansLiver CirrhosisPatient SelectionTranslational Research, BiomedicalCIRRHOSISEXTRACELLULAR MATRIXFATTY LIVERHEPATIC FIBROSISHEPATIC STELLATE CELL

Identifiers

PMID25681399
PMCPMC4477794
OpenAlexW2171925512

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.