Evidence map›Paper›PMID 26121236›Full record

ReviewAmerican journal of respiratory cell and molecular biology2015

Matrix metalloproteinases as therapeutic targets for idiopathic pulmonary fibrosis.

Vanessa J Craig, Li Zhang, James S Hagood, Caroline A Owen

Open access · greenAbstract readReview
In one paragraph

Review in American journal of respiratory cell and molecular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 285 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
285citing papers in PubMed, 3 pooled it
16.0field-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

285 citing papers in PubMed, 3 syntheses or guidelines pooled it, 504 citations in OpenAlex.

  1. Pooled it
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  16. Immunological mechanisms and therapeutic approaches in pulmonary fibrosis.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
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225 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

4 authors at 2 institutions in 1 country.

Vanessa J Craig1 Division of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital/Harvard Medical School, Boston, Massachusetts.
Li Zhang1 Division of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital/Harvard Medical School, Boston, Massachusetts.
James S Hagood3 Division of Pediatric Respiratory Medicine, University of California-San Diego, La Jolla, California, and.
Caroline A Owen1 Division of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital/Harvard Medical School, Boston, Massachusetts.
Brigham and Women's Hospital · USUniversity of California San Diego · US

Funding

XENOBIOTIC BIOTRANSFORMATION AND DISPOSITIONP30ES007033 · NIEHS · UNIVERSITY OF WASHINGTON · PI Sheela Sathyanarayana · 1995 to 2026
$42.5M
Respiratory Computational Discovery CoreP01HL114501 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI CHOI, MARY E · 2013 to 2025
$24.9M
RESPIRATORY RESEARCHT32HL007633 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI George R Washko · 1985 to 2026
$14.9M
Systems Biology, Bioinformatics, and BiostatisticsP01HL105339 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI SILVERMAN, EDWIN K · 2011 to 2015
$12.2M
Targeting MMP9 to Improve Outcomes in Serious Influenza InfectionsR01AI111475 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI HARROD, KEVIN S, LEVY, BRUCE D · 2014 to 2018
$4.3M
Novel Roles for MMP-8 in Acute Lung InjuryR01HL063137 · NHLBI · UNIVERSITY OF UTAH · PI OWEN, CAROLINE A · 1999 to 2008
$2.6M
Novel Roles for ADAM15 in Acute Lung InjuryR01HL086814 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI OWEN, CAROLINE A · 2007 to 2010
$1.6M
Novel Anti-inflammatory Activities For ADAM8 In Pulmonary EmphysemaR21HL111835 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI OWEN, CAROLINE A · 2012 to 2013
$456k
NHLBI NIH HHS HL063137NHLBI NIH HHS HL086814NHLBI NIH HHS HL105339NHLBI NIH HHS HL111835NHLBI NIH HHS HL114501NHLBI NIH HHS P01 HL105339NHLBI NIH HHS P01 HL114501NHLBI NIH HHS R01 HL063137NHLBI NIH HHS R01 HL086814NHLBI NIH HHS R21 HL111835NHLBI NIH HHS T32 HL007633NIAID NIH HHS AI111475-01NIAID NIH HHS R01 AI111475NIEHS NIH HHS P30 ES007033PHS HHS CIA123046
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a restrictive lung disease that is associated with high morbidity and mortality. Current medical therapies are not fully effective at limiting mortality in patients with IPF, and new therapies are urgently needed. Matrix metalloproteinases (MMPs) are proteinases that, together, can degrade all components of the extracellular matrix and numerous nonmatrix proteins. MMPs and their inhibitors, tissue inhibitors of MMPs (TIMPs), have been implicated in the pathogenesis of IPF based upon the results of clinical studies reporting elevated levels of MMPs (including MMP-1, MMP-7, MMP-8, and MMP-9) in IPF blood and/or lung samples. Surprisingly, studies of gene-targeted mice in murine models of pulmonary fibrosis (PF) have demonstrated that most MMPs promote (rather than inhibit) the development of PF and have identified diverse mechanisms involved. These mechanisms include MMPs: (1) promoting epithelial-to-mesenchymal transition (MMP-3 and MMP-7); (2) increasing lung levels or activity of profibrotic mediators or reducing lung levels of antifibrotic mediators (MMP-3, MMP-7, and MMP-8); (3) promoting abnormal epithelial cell migration and other aberrant repair processes (MMP-3 and MMP-9); (4) inducing the switching of lung macrophage phenotypes from M1 to M2 types (MMP-10 and MMP-28); and (5) promoting fibrocyte migration (MMP-8). Two MMPs, MMP-13 and MMP-19, have antifibrotic activities in murine models of PF, and two MMPs, MMP-1 and MMP-10, have the potential to limit fibrotic responses to injury. Herein, we review what is known about the contributions of MMPs and TIMPs to the pathogenesis of IPF and discuss their potential as therapeutic targets for IPF.

Indexed as

AnimalsCell MovementDisease Models, AnimalEpithelial-Mesenchymal TransitionExtracellular MatrixGene Expression RegulationHumansIdiopathic Pulmonary FibrosisLungMacrophages, AlveolarMatrix Metalloproteinase InhibitorsMatrix Metalloproteinases, SecretedMiceMolecular Targeted TherapyRandomized Controlled Trials as TopicSignal TransductionMatrix Metalloproteinase InhibitorsMatrix Metalloproteinases, Secretedfibrosisidiopathic pulmonary fibrosisinterstitial lung diseaselungmatrix metalloproteinase

Identifiers

PMID26121236
PMCPMC4742954
OpenAlexW1676246072

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.