Evidence map›Paper›PMID 25064447›Full record

ArticleBMC pulmonary medicine2014

Lung fibrotic tenascin-C upregulation is associated with other extracellular matrix proteins and induced by TGFβ1.

Susanna Estany, Vanesa Vicens-Zygmunt, Roger Llatjós, Ana Montes, Rosa Penín, Ignacio Escobar, Antoni Xaubet, Salud Santos, Frederic Manresa, Jordi Dorca and 1 more

Open access · goldAbstract read
In one paragraph

Article in BMC pulmonary medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 1 pooled it
4.6field-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

66 citing papers in PubMed, 1 synthesis or guideline pooled it, 102 citations in OpenAlex.

  1. Pooled it
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  7. Article
  8. Deciphering the Tenascin-C Nexus: A Comprehensive Review of Its Involvement in Chronic Respiratory Diseases.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025
    Review
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6 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 4 institutions in 1 country.

Susanna Estany
Vanesa Vicens-Zygmunt
Roger Llatjós
Ana Montes
Rosa Penín
Ignacio Escobar
Antoni Xaubet
Salud Santos
Frederic Manresa
Jordi Dorca
Maria Molina-MolinaRespiratory Research Group, IDIBELL, University of Barcelona, Barcelona, Spain. mariamolinamolina@hotmail.com.
Bellvitge University Hospital · ESUniversitat de Barcelona · ESHospital Clínic de Barcelona · ESInstitut d'Investigació Biomédica de Bellvitge · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIdiopathic pulmonary fibrosis (IPF) is a progressive parenchymal lung disease of unknown aetiology and poor prognosis, characterized by altered tissue repair and fibrosis. The extracellular matrix (ECM) is a critical component in regulating cellular homeostasis and appropriate wound healing. The aim of our study was to determine the expression profile of highlighted ECM proteins in IPF lungs.

methodsECM gene and protein expression was analyzed by cDNA microarrays, rt-PCR, immunohistochemistry and western-blot in lungs from idiopathic pulmonary fibrosis (IPF), hypersensitivity pneumonitis (HP), categorized as chronic (cHP) and subacute (saHP), and healthy lung tissue. Primary fibroblast cultures from normal subjects and fibrotic patients were studied to evaluate tenascin-C (TNC) synthesis.

resultsA total of 20 ECM proteins were upregulated and 6 proteins downregulated in IPF. TNC was almost undetected in normal lungs and significantly upregulated in fibrotic lungs (IPF and cHP) compared to saHP. Furthermore, it was located specifically in the fibroblastic foci areas of the fibrotic lung with a subepithelial gradient pattern. TNC levels were correlated with fibroblastic foci content in cHP lungs. Versican and fibronectin glycoproteins were associated with TNC, mainly in fibroblastic foci of fibrotic lungs. Fibroblasts from IPF patients constitutively synthesized higher levels of TNC than normal fibroblasts. TNC and α-sma was induced by TGF-β1 in both fibrotic and normal fibroblasts. TNC treatment of normal and fibrotic fibroblasts induced a non-significant increased α-sma mRNA.

conclusionsThe difference in ECM glycoprotein content in interstitial lung diseases could contribute to the development of lung fibrosis. The increase of TNC in interstitial areas of fibrotic activity could play a key role in the altered wound healing.

Indexed as

ActinsAdultAgedAlveolitis, Extrinsic AllergicCells, CulturedChronic DiseaseDown-RegulationFemaleFibroblastsFibronectinsGene ExpressionHumansIdiopathic Pulmonary FibrosisLungMaleMiddle AgedACTA2 protein, humanActinsFibronectinsRNA, MessengerTenascinTransforming Growth Factor beta1Versicans

Identifiers

PMID25064447
PMCPMC4123829
OpenAlexW2019072375

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.