Evidence map›Paper›PMID 24850426›Full record

ArticleMucosal immunology2014

Inhibition of a novel fibrogenic factor Tl1a reverses established colonic fibrosis.

D Q Shih, L Zheng, X Zhang, H Zhang, Y Kanazawa, R Ichikawa, K L Wallace, J Chen, C Pothoulakis, H W Koon and 1 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Mucosal immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 1 pooled it
4.8field-weighted citation impact, top 5% 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

69 citing papers in PubMed, 1 synthesis or guideline pooled it, 103 citations in OpenAlex.

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  5. 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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9 more citing papers are in PubMed but not listed here.

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

11 authors at 2 institutions in 2 countries.

D Q ShihF. Widjaja Foundation, Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, California, USA.
L Zheng1] F. Widjaja Foundation, Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, California, USA [2] Department of Gastroenterology, The Second Hospital of Hebei Medical University, Hebei, China.
X ZhangDepartment of Gastroenterology, The Second Hospital of Hebei Medical University, Hebei, China.
H Zhang1] F. Widjaja Foundation, Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, California, USA [2] Department of Gastroenterology, The Second Hospital of Hebei Medical University, Hebei, China.
Y KanazawaF. Widjaja Foundation, Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, California, USA.
R IchikawaF. Widjaja Foundation, Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, California, USA.
K L WallaceF. Widjaja Foundation, Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, California, USA.
J ChenF. Widjaja Foundation, Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, California, USA.
C PothoulakisIBD Center, David Geffen School of Medicine, UCLA, Los Angeles, California, USA.
H W KoonIBD Center, David Geffen School of Medicine, UCLA, Los Angeles, California, USA.
S R TarganF. Widjaja Foundation, Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Cedars-Sinai Medical Center · USHebei Medical University · CN

Funding

UCLA Clinical and Translational Science InstituteUL1TR000124 · NCATS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DUBINETT, STEVEN M. · 2012 to 2015
$57.0M
Using polygenic scores to enhance both variant discovery, and understanding of functional consequences of genetic variation in IBD.P01DK046763 · NIDDK · CEDARS-SINAI MEDICAL CENTER · PI TARGAN, STEPHAN R. · 1992 to 2020
$31.1M
Pilot and Feasibility ProgramP30DK041301 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ROZENGURT, JUAN ENRIQUE · 1990 to 2019
$18.0M
TNF ALPHA AND CROHNS DISEASE MUCOSAL INFLAMMATIONR01DK056328 · NIDDK · CEDARS-SINAI MEDICAL CENTER · PI TARGAN, STEPHAN R. · 1999 to 2018
$6.9M
The Roles of IBD Associated Genes ATG16L1 and TNFSF15 in Gut Mucosal InflammationK08DK093578 · NIDDK · CEDARS-SINAI MEDICAL CENTER · PI SHIH, DAVID Q. · 2012 to 2016
$755k
NCATS NIH HHS UL1 TR000124NCATS NIH HHS UL1TR000124NIDDK NIH HHS DK056328NIDDK NIH HHS DK093578NIDDK NIH HHS K08 DK093578NIDDK NIH HHS P01 DK046763NIDDK NIH HHS P30 DK041301NIDDK NIH HHS R01 DK056328
6 · The paper itself

Abstract

Intestinal fibrostenosis is among the hallmarks of severe Crohn's disease. Patients with certain TNFSF15 (gene name for TL1A) variants over-express TL1A and have a higher risk of developing strictures in the small intestine. In addition, sustained Tl1a expression in mice leads to small and large intestinal fibrostenosis under colitogenic conditions. The aim of this study was to determine whether established murine colonic fibrosis could be reversed with Tl1a antibody (Ab). Treatment with neutralizing Tl1a Ab reversed colonic fibrosis back to the original pre-inflamed levels, potentially as a result of lowered expression of connective tissue growth factor, Il31Ra, transforming growth factor β1 and insulin-like growth factor-1. In addition, blocking Tl1a function by either neutralizing Tl1a Ab or deletion of death domain receptor 3 (Dr3) reduced the number of fibroblasts and myofibroblasts, the primary cell types that mediate tissue fibrosis. Primary intestinal myofibroblasts expressed Dr3 and functionally responded to direct Tl1a signaling by increasing collagen and Il31Ra expression. These data demonstrated a direct role for TL1A-DR3 signaling in tissue fibrosis and that modulation of TL1A-DR3 signaling could inhibit gut fibrosis.

Indexed as

AnimalsAntibodies, NeutralizingColonCrohn DiseaseFibrosisHumansMiceMice, KnockoutMyofibroblastsReceptors, InterleukinReceptors, Tumor Necrosis Factor, Member 25Signal TransductionTumor Necrosis Factor Ligand Superfamily Member 15Antibodies, NeutralizingIL31RA protein, humanIl31ra protein, mouseReceptors, InterleukinReceptors, Tumor Necrosis Factor, Member 25TNFRSF25 protein, humanTnfrsf25 protein, mouseTNFSF15 protein, humanTnfsf15 protein, mouseTumor Necrosis Factor Ligand Superfamily Member 15

Identifiers

PMID24850426
PMCPMC4205266
OpenAlexW1992752307

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.