Evidence map›Paper›PMID 39026298›Full record

ReviewStem cell research & therapy2024

Epicardial EMT and cardiac repair: an update.

Eleonora Foglio, Erica D'Avorio, Riccardo Nieri, Matteo Antonio Russo, Federica Limana

Abstract readReview
In one paragraph

Review in Stem cell research & therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–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

13 citing papers in PubMed.

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  11. Epicardium-myocardium crosstalk orchestrates heart development.Frontiers in cell and developmental biology · 2025
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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

5 authors.

Eleonora FoglioTechnoscience, Parco Scientifico e Tecnologico Pontino, Latina, Italy.
Erica D'AvorioDipartimento di Promozione delle Scienze Umane e della Qualità della Vita, San Raffaele University of Rome, Rome, Italy.
Riccardo NieriDepartment of Experimental Medicine, Sapienza University of Rome, Rome, Italy.
Matteo Antonio RussoIRCCS San Raffaele Roma, Rome, Italy.
Federica LimanaDipartimento di Promozione delle Scienze Umane e della Qualità della Vita, San Raffaele University of Rome, Rome, Italy. federica.limana@uniroma5.it.ORCID 0000-0002-8606-9628

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epicardial epithelial-to-mesenchymal transition (EMT) plays a pivotal role in both heart development and injury response and involves dynamic cellular changes that are essential for cardiogenesis and myocardial repair. Specifically, epicardial EMT is a crucial process in which epicardial cells lose polarity, migrate into the myocardium, and differentiate into various cardiac cell types during development and repair. Importantly, following EMT, the epicardium becomes a source of paracrine factors that support cardiac growth at the last stages of cardiogenesis and contribute to cardiac remodeling after injury. As such, EMT seems to represent a fundamental step in cardiac repair. Nevertheless, endogenous EMT alone is insufficient to stimulate adequate repair. Redirecting and amplifying epicardial EMT pathways offers promising avenues for the development of innovative therapeutic strategies and treatment approaches for heart disease. In this review, we present a synthesis of recent literature highlighting the significance of epicardial EMT reactivation in adult heart disease patients.

Indexed as

Epithelial-Mesenchymal TransitionPericardiumAnimalsCell DifferentiationHeart DiseasesHumansMyocardiumCardiac repair and regenerationEMTEpicardial cellsMolecular rehabilitation

Identifiers

PMID39026298
PMCPMC11264588

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.