Evidence mapPaperPMID 33409282Full record

ReviewFrontiers in cell and developmental biology2020

The Epithelial-to-Mesenchymal Transition as a Possible Therapeutic Target in Fibrotic Disorders.

Jacopo Di Gregorio, Iole Robuffo, Sonia Spalletta, Giulia Giambuzzi, Vincenzo De Iuliis, Elena Toniato, Stefano Martinotti, Pio Conti, Vincenzo Flati

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed, 1 pooled it
10.1field-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

90 citing papers in PubMed, 1 synthesis or guideline pooled it, 137 citations in OpenAlex.

  1. Pooled it
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  10. Single-cell Profiling Reveals Cooperative Participation ofInternational journal of medical sciences · 2026
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  16. The Potential Role ofMicroorganisms · 2025
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30 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

9 authors at 4 institutions in 2 countries.

Jacopo Di GregorioBurnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, FL, United States.
Iole RobuffoInstitute of Molecular Genetics, National Research Council, Section of Chieti, Chieti, Italy.
Sonia SpallettaDepartment of Clinical Pathology, E. Profili Hospital, Fabriano, Ancona, Italy.
Giulia GiambuzziDepartment of Medical and Oral Sciences and Biotechnologies, University "G. d'Annunzio", Chieti, Italy.
Vincenzo De IuliisDepartment of Medical and Oral Sciences and Biotechnologies, University "G. d'Annunzio", Chieti, Italy.
Elena ToniatoDepartment of Medical and Oral Sciences and Biotechnologies, University "G. d'Annunzio", Chieti, Italy.
Stefano MartinottiDepartment of Medical and Oral Sciences and Biotechnologies, University "G. d'Annunzio", Chieti, Italy.
Pio ContiPostgraduate Medical School, University of Chieti-Pescara, Chieti, Italy.
Vincenzo FlatiDepartment of Biotechnological and Applied Clinical Sciences, University of L'Aquila, L'Aquila, Italy.
University of Chieti-Pescara · ITNational Research Council · ITUniversity of Central Florida · USUniversity of L'Aquila · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibrosis is a chronic and progressive disorder characterized by excessive deposition of extracellular matrix, which leads to scarring and loss of function of the affected organ or tissue. Indeed, the fibrotic process affects a variety of organs and tissues, with specific molecular background. However, two common hallmarks are shared: the crucial role of the transforming growth factor-beta (TGF-β) and the involvement of the inflammation process, that is essential for initiating the fibrotic degeneration. TGF-β in particular but also other cytokines regulate the most common molecular mechanism at the basis of fibrosis, the Epithelial-to-Mesenchymal Transition (EMT). EMT has been extensively studied, but not yet fully explored as a possible therapeutic target for fibrosis. A deeper understanding of the crosstalk between fibrosis and EMT may represent an opportunity for the development of a broadly effective anti-fibrotic therapy. Here we report the evidences of the relationship between EMT and multi-organ fibrosis, and the possible therapeutic approaches that may be developed by exploiting this relationship.

Indexed as

autophagyEMTfibrosisinflammationSMADsTGF-βWnt

Identifiers

PMID33409282
PMCPMC7779530
OpenAlexW3117344389

What Socratic 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 Socratic graph.