Evidence map›Paper›PMID 33202716›Full record

ArticleMedicina (Kaunas, Lithuania)2020

Epithelial-Mesenchymal Transition: A Major Pathogenic Driver in Idiopathic Pulmonary Fibrosis?

Francesco Salton, Barbara Ruaro, Paola Confalonieri, Marco Confalonieri

Abstract readEditorial
In one paragraph

Article in Medicina (Kaunas, Lithuania), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

52 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
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  7. Targeting the epithelium in pulmonary fibrosis.European respiratory review : an official journal of the European Respiratory Society · 2026
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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

4 authors.

Francesco SaltonPulmonology Department, University Hospital of Cattinara, 34149 Trieste, Italy.ORCID 0000-0002-0864-9766
Barbara RuaroPulmonology Department, University Hospital of Cattinara, 34149 Trieste, Italy.
Paola ConfalonieriPulmonology Department, University Hospital of Cattinara, 34149 Trieste, Italy.
Marco ConfalonieriPulmonology Department, University Hospital of Cattinara, 34149 Trieste, Italy.ORCID 0000-0002-4791-768X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite the fact that epithelial-mesenchymal transition (EMT) is a common downstream mechanism of all fibrosing diseases, whether it represents a leading process in the development of idiopathic pulmonary fibrosis has been widely discussed and is still a matter of debate. According to the most recent advances, EMT is thought to be mainly driven by the overexpression of several developmental pathways upstream of dysfunctional epithelial regeneration, which indeed normally occurs after damage and during tissue turnover. Future research should likely be directed at investigating the molecular mechanisms underlying epithelial dysfunction, in order to allow for both the removal of the wording "idiopathic" from idiopathic pulmonary fibrosis ("IPF") and for the identification of earlier and more effective therapeutic targets than the late process of fibrosis.

Indexed as

Epithelial-Mesenchymal TransitionIdiopathic Pulmonary FibrosisFibrosisHumans

Identifiers

PMID33202716
PMCPMC7697350

What OpenQuestion holds

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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.