Evidence map›Paper›PMID 31296856›Full record

ArticleNature communications2019

Regulation of tumor angiogenesis and mesenchymal-endothelial transition by p38α through TGF-β and JNK signaling.

Raquel Batlle, Eva Andrés, Lorena Gonzalez, Elisabet Llonch, Ana Igea, Núria Gutierrez-Prat, Antoni Berenguer-Llergo, Angel R Nebreda

Open access · goldAbstract readVideo-Audio Media
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed
8.2field-weighted citation impact, top 2% 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

89 citing papers in PubMed, 150 citations in OpenAlex.

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  14. The role of JNK signaling pathway in organ fibrosis.Journal of advanced research · 2025
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29 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

8 authors at 2 institutions in 1 country.

Raquel BatlleInstitute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, 08028, Barcelona, Spain.ORCID http://orcid.org/0000-0003-3366-1393
Eva AndrésInstitute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, 08028, Barcelona, Spain.
Lorena GonzalezInstitute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, 08028, Barcelona, Spain.
Elisabet LlonchInstitute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, 08028, Barcelona, Spain.
Ana IgeaInstitute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, 08028, Barcelona, Spain.
Núria Gutierrez-PratInstitute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, 08028, Barcelona, Spain.
Antoni Berenguer-LlergoInstitute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, 08028, Barcelona, Spain.ORCID http://orcid.org/0000-0002-3742-8161
Angel R NebredaInstitute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, 08028, Barcelona, Spain. angel.nebreda@irbbarcelona.org.
Institute for Research in Biomedicine · ESInstitució Catalana de Recerca i Estudis Avançats · ES

Funding

Departament d'Innovació, Universitats i Empresa, Generalitat de Catalunya (Department of Innovation, Education and Enterprise, Government of Catalonia) 2017 SGR-557EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 European Research Council (H2020 Excellent Science - European Research Council) ERC 294665Fundació la Marató de TV3 (TV3 Marathon Foundation) 20133430Ministerio de Economía y Competitividad (Ministry of Economy and Competitiveness) SAF2016-81043-R
6 · The paper itself

Abstract

The formation of new blood vessels is essential for normal development, tissue repair and tumor growth. Here we show that inhibition of the kinase p38α enhances angiogenesis in human and mouse colon tumors. Mesenchymal cells can contribute to tumor angiogenesis by regulating proliferation and migration of endothelial cells. We show that p38α negatively regulates an angiogenic program in mesenchymal stem/stromal cells (MSCs), multipotent progenitors found in perivascular locations. This program includes the acquisition of an endothelial phenotype by MSCs mediated by both TGF-β and JNK, and negatively regulated by p38α. Abrogation of p38α in mesenchymal cells increases tumorigenesis, which correlates with enhanced angiogenesis. Using genetic models, we show that p38α regulates the acquisition of an endothelial-like phenotype by mesenchymal cells in colon tumors and damage tissue. Taken together, our results indicate that p38α in mesenchymal cells restrains a TGF-β-induced angiogenesis program including their ability to transdifferentiate into endothelial cells.

Indexed as

AnimalsAzoxymethaneCarcinogensCell ProliferationCell TransdifferentiationColonic NeoplasmsEndothelial CellsEndothelium, VascularEpithelial-Mesenchymal TransitionGene Knockdown TechniquesHT29 CellsHumansJNK Mitogen-Activated Protein KinasesMAP Kinase Signaling SystemMesenchymal Stem CellsMiceAzoxymethaneCarcinogensJNK Mitogen-Activated Protein KinasesMitogen-Activated Protein Kinase 14RNA, Small InterferingTransforming Growth Factor beta

Identifiers

PMID31296856
PMCPMC6624205
OpenAlexW2962661158

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.