Evidence map›Paper›PMID 12466116›Full record

ArticleThe American journal of pathology2002

Increased carbon tetrachloride-induced liver injury and fibrosis in FGFR4-deficient mice.

Chundong Yu, Fen Wang, Chengliu Jin, Xiaochong Wu, Wai-kin Chan, Wallace L McKeehan

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

47 citing papers in PubMed, 122 citations in OpenAlex.

  1. Identification of IPF specific genes expressed by lung tissue-derived fibroblasts using next generation sequencing.Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG · 2026
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  14. Editorial: Resident and Ectopic FGF Signaling in Development and Disease.Frontiers in cell and developmental biology · 2020
    Article
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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 2 institutions in 1 country.

Chundong YuDepartment of Biochemistry and Biophysics, Institute of Biosciences and Technology, Texas A&M University System Health Science Center, 2121 W. Holcombe Boulevard, Houston, TX 77030-3303, USA.
Fen Wang
Chengliu Jin
Xiaochong Wu
Wai-kin Chan
Wallace L McKeehan
Texas A&M University System · USThe University of Texas Health Science Center at Houston · US

Funding

HUMAN HEPATOCYTE GROWTH FACTORSR01DK035310 · NIDDK · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI MCKEEHAN, WALLACE LEE · 1986 to 2006
$1.9M
Mechanism of action of STAMP - a new comodulator of glucocorticoid receptorsZ01DK047039 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI SIMONS, S STONEY · 2007 to 2008
$536k
Intramural NIH HHS Z01 DK047039NIDDK NIH HHS DK 35310NIDDK NIH HHS DK 47039NIDDK NIH HHS R01 DK035310
6 · The paper itself

Abstract

Carbon tetrachloride (CCl(4)) intoxification in rodents is a commonly used model of both acute and chronic liver injury. Recently, we showed that mice in which FGFR4 was ablated from the germline exhibited elevated cholesterol metabolism and bile acid synthesis coincident with unrepressed levels of cytochrome P450 7A (CYP7A), the rate-limiting enzyme in cholesterol disposal. Of the four fibroblast growth factor (FGF) receptor genes expressed in adult liver, FGFR4 is expressed specifically in mature hepatocytes. To determine whether FGFR4 plays a broader role in liver-specific metabolic functions, we examined the impact of both acute and chronic exposure to CCl(4) in FGFR4-deficient mice. Following acute CCl(4) exposure, the FGFR4-deficient mice exhibited accelerated liver injury, a significant increase in liver mass and delayed hepatolobular repair. Chronic CCl(4) exposure resulted in severe fibrosis in livers of FGFR4-deficient mice compared to normal mice. Analysis at both mRNA and protein levels indicated an 8-hour delay in FGFR4-deficient mice in the down-regulation of cytochrome P450 2E1 (CYP2E1) protein, the major enzyme whose products underlie CCl(4)-induced injury. These results show that hepatocyte FGFR4 protects against acute and chronic insult to the liver and prevents accompanying fibrosis. The results show that FGFR4 acts by promotion of processes that restore hepatolobular architecture rather than cellularity while limiting damage due to prolonged CYP2E1 activity.

Indexed as

Alanine TransaminaseAnimalsCarbon TetrachlorideCyclic AMP-Dependent Protein KinasesCytochrome P-450 CYP2E1Down-RegulationFemaleHepatocytesLiverLiver CirrhosisMiceMice, KnockoutReceptor, Fibroblast Growth Factor, Type 4Receptors, Fibroblast Growth FactorUrokinase-Type Plasminogen ActivatorAlanine TransaminaseCarbon TetrachlorideCyclic AMP-Dependent Protein KinasesCytochrome P-450 CYP2E1Fgfr4 protein, mouseReceptor, Fibroblast Growth Factor, Type 4Receptors, Fibroblast Growth FactorUrokinase-Type Plasminogen Activator

Identifiers

PMID12466116
PMCPMC1850898
OpenAlexW2142741880

What OpenQuestion holds

Textmetadata
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.