Evidence map›Paper›PMID 34338295›Full record

ArticleJournal of cell science2021

A dual role of YAP in driving TGFβ-mediated endothelial-to-mesenchymal transition.

Cecilia Savorani, Matteo Malinverno, Roberta Seccia, Claudio Maderna, Monica Giannotta, Linda Terreran, Eleonora Mastrapasqua, Stefano Campaner, Elisabetta Dejana, Costanza Giampietro

Open access · hybridAbstract read
In one paragraph

Article in Journal of cell science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

18 citing papers in PubMed, 24 citations in OpenAlex.

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  5. Endothelial to mesenchymal transition: a central mechanism in diabetes-induced vascular pathology.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 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

10 authors at 4 institutions in 3 countries.

Cecilia SavoraniInstitute of Molecular Oncology (IFOM), The Fondazione Italiana per la Ricerca sul Cancro (FIRC) Institute of Molecular Oncology, Milan 20139, Italy.ORCID 0000-0002-8096-1148
Matteo MalinvernoInstitute of Molecular Oncology (IFOM), The Fondazione Italiana per la Ricerca sul Cancro (FIRC) Institute of Molecular Oncology, Milan 20139, Italy.ORCID 0000-0001-8242-7937
Roberta SecciaInstitute of Molecular Oncology (IFOM), The Fondazione Italiana per la Ricerca sul Cancro (FIRC) Institute of Molecular Oncology, Milan 20139, Italy.ORCID 0000-0001-6021-3524
Claudio MadernaInstitute of Molecular Oncology (IFOM), The Fondazione Italiana per la Ricerca sul Cancro (FIRC) Institute of Molecular Oncology, Milan 20139, Italy.
Monica GiannottaInstitute of Molecular Oncology (IFOM), The Fondazione Italiana per la Ricerca sul Cancro (FIRC) Institute of Molecular Oncology, Milan 20139, Italy.
Linda TerreranInstitute of Molecular Oncology (IFOM), The Fondazione Italiana per la Ricerca sul Cancro (FIRC) Institute of Molecular Oncology, Milan 20139, Italy.ORCID 0000-0002-1089-3813
Eleonora MastrapasquaInstitute of Molecular Oncology (IFOM), The Fondazione Italiana per la Ricerca sul Cancro (FIRC) Institute of Molecular Oncology, Milan 20139, Italy.ORCID 0000-0001-6507-7998
Stefano CampanerCenter for Genomic Science of IIT@SEMM, Fondazione Istituto Italiano di Tecnologia (IIT), Milan 20139, Italy.
Elisabetta DejanaInstitute of Molecular Oncology (IFOM), The Fondazione Italiana per la Ricerca sul Cancro (FIRC) Institute of Molecular Oncology, Milan 20139, Italy.
Costanza GiampietroInstitute of Molecular Oncology (IFOM), The Fondazione Italiana per la Ricerca sul Cancro (FIRC) Institute of Molecular Oncology, Milan 20139, Italy.ORCID 0000-0001-5229-3835
IFOM · ITETH Zurich · CHItalian Institute of Technology · ITUppsala University · SE

Funding

European Research Council EC-ERC-VEPCMarie Curie ITN-2012-317250Swiss National Science FoundationTelethon GGP19202
6 · The paper itself

Abstract

Endothelial-to-mesenchymal transition (EndMT) is the biological process through which endothelial cells transdifferentiate into mesenchymal cells. During embryo development, EndMT regulates endocardial cushion formation via TGFβ/BMP signaling. In adults, EndMT is mainly activated during pathological conditions. Hence, it is necessary to characterize molecular regulators cooperating with TGFβ signaling in driving EndMT, to identify potential novel therapeutic targets to treat these pathologies. Here, we studied YAP, a transcriptional co-regulator involved in several biological processes, including epithelial-to-mesenchymal transition (EMT). As EndMT is the endothelial-specific form of EMT, and YAP (herein referring to YAP1) and TGFβ signaling cross-talk in other contexts, we hypothesized that YAP contributes to EndMT by modulating TGFβ signaling. We demonstrate that YAP is required to trigger TGFβ-induced EndMT response, specifically contributing to SMAD3-driven EndMT early gene transcription. We provide novel evidence that YAP acts as SMAD3 transcriptional co-factor and prevents GSK3β-mediated SMAD3 phosphorylation, thus protecting SMAD3 from degradation. YAP is therefore emerging as a possible candidate target to inhibit pathological TGFβ-induced EndMT at early stages.

Indexed as

Endothelial CellsTransforming Growth Factor betaEpithelial-Mesenchymal TransitionPhosphorylationTransforming Growth Factor betaEndothelial-to-mesenchymal transitionSMAD3TGFβ pathwayYAP

Identifiers

PMID34338295
PMCPMC8353525
OpenAlexW3192874168

What OpenQuestion holds

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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.