Evidence map›Paper›PMID 29625182›Full record

ReviewMatrix biology : journal of the International Society for Matrix Biology2018

Idiopathic pulmonary fibrosis: Epithelial-mesenchymal interactions and emerging therapeutic targets.

Justin C Hewlett, Jonathan A Kropski, Timothy S Blackwell

Open access · greenAbstract readReview
In one paragraph

Review in Matrix biology : journal of the International Society for Matrix Biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 176 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
176citing papers in PubMed, 4 pooled it
12.5field-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

176 citing papers in PubMed, 4 syntheses or guidelines pooled it, 329 citations in OpenAlex.

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116 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

3 authors at 1 institution in 1 country.

Justin C HewlettDivision of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, United States.
Jonathan A KropskiDivision of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, United States; Department of Veterans Affairs Medical Center, Nashville, TN, United States. Electronic address: jon.kropski@vanderbilt.edu.
Timothy S BlackwellDivision of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, United States; Department of Veterans Affairs Medical Center, Nashville, TN, United States; Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, TN, United States. Electronic address: timothy.blackwell@vanderbilt.edu.
Vanderbilt University Medical Center · US

Funding

Mechanisms of Familial Pulmonary FibrosisP01HL092870 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BLACKWELL, TIMOTHY S. · 2010 to 2020
$21.6M
Interdisciplinary Training Program in Lung ResearchT32HL094296 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Ray Stokes Peebles · 2008 to 2026
$6.3M
Epithelial-Fibroblast Interactions in Lung FibrosisR01HL085317 · NHLBI · VANDERBILT UNIVERSITY · PI BLACKWELL, TIMOTHY S. · 2007 to 2015
$3.5M
DNA-Damage Repair In Pulmonary FibrosisK08HL130595 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI KROPSKI, JONATHAN ANDREW · 2016 to 2020
$786k
Mechanisms driving airway inflammation in chronic lung diseaseI01BX002378 · VA · VETERANS HEALTH ADMINISTRATION · PI Timothy S. Blackwell · 2014 to 2026
–
BLRD VA I01 BX002378NHLBI NIH HHS K08 HL130595NHLBI NIH HHS P01 HL092870NHLBI NIH HHS R01 HL085317NHLBI NIH HHS T32 HL094296
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a chronic fibrotic disease of the lung that is marked by progressive decline in pulmonary function and ultimately respiratory failure. Genetic and environmental risk factors have been identified that indicate injury to, and dysfunction of the lung epithelium is central to initiating the pathogenic process. Following injury to the lung epithelium, growth factors, matrikines and extracellular matrix driven signaling together activate a variety of repair pathways that lead to inflammatory cell recruitment, fibroblast proliferation and expansion of the extracellular matrix, culminating in tissue fibrosis. This tissue fibrosis then leads to changes in the biochemical and biomechanical properties of the extracellular matrix, which potentiate profibrotic mechanisms through a "feed-forward cycle." This review provides an overview of the interactions of the pathogenic mechanisms of IPF with a focus on epithelial-mesenchymal crosstalk and the extracellular matrix as a therapeutic target for idiopathic pulmonary fibrosis.

Indexed as

Epithelial-Mesenchymal TransitionExtracellular MatrixHumansIdiopathic Pulmonary FibrosisLungMolecular Targeted TherapySignal TransductionGeneticsInterstitial lung diseaseIPFMatrixTreatment

Identifiers

PMID29625182
PMCPMC6146058
OpenAlexW2795718114

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.