Evidence map›Paper›PMID 28405672›Full record

ArticleThrombosis and haemostasis2017

Glucagon-like peptide 1-related peptides increase nitric oxide effects to reduce platelet activation.

Cristina Barale, Simona Buracco, Franco Cavalot, Chiara Frascaroli, Angelo Guerrasio, Isabella Russo

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Thrombosis and haemostasis, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 9% 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

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.

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  18. Incretin-based therapy: a new horizon in diabetes management.Journal of diabetes and metabolic disorders · 2024
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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

6 authors at 2 institutions in 1 country.

Cristina Barale
Simona Buracco
Franco Cavalot
Chiara Frascaroli
Angelo Guerrasio
Isabella RussoDr. Isabella Russo, PhD, Internal Medicine and Metabolic Disease Unit, Department of Clinical and Biological Sciences of the Turin University, San Luigi Gonzaga Hospital, 10043 Orbassano (Turin), Italy, Tel.: + 39 011 9026622, Fax: + 39 011 9038639, E-mail: isabella.russo@unito.it.
Ospedale San Luigi Gonzaga · ITUniversity of Turin · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glucagon-like peptide 1 (GLP-1) is object of intensive investigation for not only its metabolic effects but also the protective vascular actions. Since platelets exert a primary role in the pathogenesis of atherosclerosis, inflammation and vascular complications, we investigated whether GLP-1 directly influences platelet reactivity. For this purpose, in platelets from 72 healthy volunteers we evaluated GLP-1 receptor (GLP-1R) expression and the effects of a 15-minute incubation with the native form GLP-1(7-36), the N-terminally truncated form GLP-1(9-36) and the GLP-1 analogue Liraglutide (100 nmol/l) on: i) aggregation induced by collagen or arachidonic acid (AA); ii) platelet function under shear stress; iii) cGMP and cAMP synthesis and cGMP-dependent protein kinase (PKG)-induced Vasodilator-Stimulated-Phosphoprotein (VASP) phosphorylation; iv) activation of the signalling molecules Phosphatidylinositol 3-Kinase (PI3-K)/Akt and Mitogen Activated Protein Kinase (MAPK)/ERK-1/2; and v) oxidative stress. Experiments were repeated in the presence of the nitric oxide donor Na-nitroprusside. We found that platelets constitutively express GLP-1R and that, independently of GLP-1R, GLP-1(7-36), GLP-1(9-36) and Liraglutide exert platelet inhibitory effects as shown by: a) increased NO-antiaggregating effects, b) increased the activation of the cGMP/PKG/VASP pathway, c) reduced the activation of PI3-K/Akt and MAPK/ERK-2 pathways, d) reduced the AA-induced oxidative stress. When the experiments were repeated in the presence of the antagonist of GLP-1R Exendin(9-39), the platelet inhibitory effects were maintained, thus indicating a mechanism independent of GLP-1R. In conclusion, GLP-1(7-36), its degradation product GLP-1(9-36) and Liraglutide exert similar inhibitory effects on platelet activation, suggesting a potential protective effect on the cardiovascular system.

Indexed as

Platelet ActivationAdultBlood PlateletsCell Adhesion MoleculesCells, CulturedCyclic GMPDiabetes Mellitus, Type 2FemaleGlucagon-Like Peptide 1Glucagon-Like Peptide-1 ReceptorHumansLiraglutideMaleMicrofilament ProteinsNitric OxideNitroprussideCell Adhesion MoleculesCyclic GMPGLP1R protein, humanGlucagon-Like Peptide 1glucagon-like peptide 1 (7-36)amideGlucagon-Like Peptide-1 ReceptorLiraglutideMicrofilament ProteinsNitric OxideNitroprussidePeptide FragmentsPhosphatidylinositol 3-KinasesPhosphoproteinsVasodilator-Stimulated Phosphoproteindiabetesglucagone-like peptide 1Liraglutidenitric oxidePlatelets

Identifiers

PMID28405672
PMCPMC6291961
OpenAlexW2606913382

What OpenQuestion holds

Texttitle and abstract
LicenceCC BY-NC-ND
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.