Evidence map›Paper›PMID 20452396›Full record

ArticleMolecular and cellular endocrinology2010

Exendin-4 stimulates proliferation of human coronary artery endothelial cells through eNOS-, PKA- and PI3K/Akt-dependent pathways and requires GLP-1 receptor.

O Erdogdu, D Nathanson, A Sjöholm, T Nyström, Q Zhang

Registry-linked trialAbstract read
PubMed Publisher
In one paragraph

Article in Molecular and cellular endocrinology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02621489 (Effects on Re-endothelialisation With Bydureon Treatment Add on to Insulin Versus Insulin Alone, Both in Combination With Metformin in Type 2 Diabetic Subjects), which is not on this map. Cited by 117 papers.

0numbers the graph read from it
0cells of the map it votes in
117citing papers in PubMed
8.9field-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.

NCT02621489 phase4completedstarted 2015, after this paper: background citation

Effects on Re-endothelialisation With Bydureon Treatment Add on to Insulin Versus Insulin Alone, Both in Combination With Metformin in Type 2 Diabetic Subjects

Ran2015Enrolled38Registered outcomes16Posted comparisons0ConditionsAtherosclerosis, Diabetes, RestenosisArmsBydureon, Humulin kwickpen, Metformin
PMID 25966620PMID 23343509PMID 23241323PMID 22390929PMID 20630463PMID 15353407other papers from this trial
Open the trial in the graph
3 · Its place in the literature

Who cites it

117 citing papers in PubMed, 223 citations in OpenAlex.

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  15. Targeting Sarcopenia in CKD: The Emerging Role of GLP-1 Receptor Agonists.International journal of molecular sciences · 2025
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  17. The Interplay Between Immunity, Inflammation and Endothelial Dysfunction.International journal of molecular sciences · 2025
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57 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

5 authors at 2 institutions in 1 country.

O ErdogduKarolinska Institutet, Department of Clinical Science and Education, Unit for Diabetes Research, Södersjukhuset, Stockholm, Sweden.
D Nathanson
A Sjöholm
T Nyström
Q Zhang
Karolinska Institutet · SEStockholm South General Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial cells have a robust capacity to proliferate and participate in angiogenesis, which underlies the maintenance of intimal layer integrity. We previously showed the presence of the GLP-1 receptor in human coronary artery endothelial cells (HCAECs) and the ameliorative actions of GLP-1 on endothelial dysfunction in type 2 diabetic patients. Here, we have studied the effect of exendin-4 on cell proliferation and its underlying mechanisms in HCAECs. Incubation of HCAECs with exendin-4 resulted in a dose-dependent increase in DNA synthesis and an increased cell number, associated with an enhanced eNOS and Akt activation, which were inhibited by PKA, PI3K, Akt or eNOS inhibitors and abolished by a GLP-1 receptor antagonist. Similar effects were obtained by applying GLP-1 (7-36) or GLP-1 (9-36). Co-incubation of exendin-4 and GLP-1 did not show additive effects. Our results suggest that exendin-4 stimulates proliferation of HCAECs through PKA-PI3K/Akt-eNOS activation pathways via a GLP-1 receptor-dependent mechanism.

Indexed as

Cell ProliferationCells, CulturedCoronary VesselsCyclic AMP-Dependent Protein KinasesDose-Response Relationship, DrugEndothelial CellsExenatideGlucagon-Like Peptide-1 ReceptorHumansMAP Kinase Signaling SystemNitric Oxide Synthase Type IIIOncogene Protein v-aktPeptidesPhosphatidylinositol 3-KinasesPhosphorylationReceptors, GlucagonCyclic AMP-Dependent Protein KinasesExenatideGLP1R protein, humanGlucagon-Like Peptide-1 ReceptorNitric Oxide Synthase Type IIINOS3 protein, humanOncogene Protein v-aktPeptidesPhosphatidylinositol 3-KinasesReceptors, GlucagonVenoms

Identifiers

PMID20452396
OpenAlexW1995209325

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.