Evidence map›Paper›PMID 31740700›Full record

ArticleScientific reports2019

Integration of TGF-β-induced Smad signaling in the insulin-induced transcriptional response in endothelial cells.

Erine H Budi, Steven Hoffman, Shaojian Gao, Ying E Zhang, Rik Derynck

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

15 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. 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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  13. Fluid shear stress generates a unique signaling response by activating multiple TGFβ family type I receptors in osteocytes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
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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 at 2 institutions in 1 country.

Erine H BudiDepartments of Cell and Tissue Biology, and Anatomy, Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, University of California at San Francisco, San Francisco, CA, 94143-0669, USA.
Steven HoffmanDepartments of Cell and Tissue Biology, and Anatomy, Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, University of California at San Francisco, San Francisco, CA, 94143-0669, USA.
Shaojian GaoThoracic and Gastrointestinal Oncology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, 20892-1906, USA.
Ying E ZhangLaboratory of Cellular and Molecular Biology, Center for Cancer Research, National Cancer Institute, Bethesda, MD, 20892-4256, USA.ORCID http://orcid.org/0000-0003-2753-7601
Rik DerynckDepartments of Cell and Tissue Biology, and Anatomy, Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, University of California at San Francisco, San Francisco, CA, 94143-0669, USA. rik.derynck@ucsf.edu.
Broad Center · USNational Cancer Institute · US

Funding

TGF-beta-induced non-Smad signaling events and cancer cell behaviorR01CA136690 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI DERYNCK, RIK M · 2009 to 2018
$3.3M
NCI NIH HHS R01 CA136690
6 · The paper itself

Abstract

Insulin signaling governs many processes including glucose homeostasis and metabolism, and is therapeutically used to treat hyperglycemia in diabetes. We demonstrated that insulin-induced Akt activation enhances the sensitivity to TGF-β by directing an increase in cell surface TGF-β receptors from a pool of intracellular TGF-β receptors. Consequently, increased autocrine TGF-β signaling in response to insulin participates in insulin-induced angiogenic responses of endothelial cells. With TGF-β signaling controlling many cell responses, including differentiation and extracellular matrix deposition, and pathologically promoting fibrosis and cancer cell dissemination, we addressed to which extent autocrine TGF-β signaling participates in insulin-induced gene responses of human endothelial cells. Transcriptome analyses of the insulin response, in the absence or presence of a TGF-β receptor kinase inhibitor, revealed substantial positive and negative contributions of autocrine TGF-β signaling in insulin-responsive gene responses. Furthermore, insulin-induced responses of many genes depended on or resulted from autocrine TGF-β signaling. Our analyses also highlight extensive contributions of autocrine TGF-β signaling to basal gene expression in the absence of insulin, and identified many novel TGF-β-responsive genes. This data resource may aid in the appreciation of the roles of autocrine TGF-β signaling in normal physiological responses to insulin, and implications of therapeutic insulin usage.

Indexed as

BenzamidesCells, CulturedDioxolesGene Expression ProfilingGene OntologyHigh-Throughput Nucleotide SequencingHumansHuman Umbilical Vein Endothelial CellsHypoglycemic AgentsInsulinReceptors, Transforming Growth Factor betaReverse Transcriptase Polymerase Chain ReactionSignal TransductionSmad3 ProteinSmad ProteinsTransforming Growth Factor beta4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamideBenzamidesDioxolesHypoglycemic AgentsInsulinReceptors, Transforming Growth Factor betaSmad3 ProteinSmad ProteinsTransforming Growth Factor beta

Identifiers

PMID31740700
PMCPMC6861289
OpenAlexW2985942578

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.