Evidence map›Paper›PMID 26807480›Full record

ArticleBiochemical pharmacology2016

Glucagon-like peptide-1 inhibits vascular smooth muscle cell dedifferentiation through mitochondrial dynamics regulation.

Gloria Torres, Pablo E Morales, Marina García-Miguel, Ignacio Norambuena-Soto, Benjamín Cartes-Saavedra, Gonzalo Vidal-Peña, David Moncada-Ruff, Fernanda Sanhueza-Olivares, Alejandra San Martín, Mario Chiong

Open access · bronzeAbstract read
In one paragraph

Article in Biochemical pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

33 citing papers in PubMed, 60 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Gut Molecules in Cardiometabolic Diseases: The Mechanisms behind the Story.International journal of molecular sciences · 2023
    Review
  16. Review
  17. Review
  18. Review
  19. Review
  20. Article
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 2 institutions in 2 countries.

Gloria TorresAdvanced Center for Chronic Diseases (ACCDiS), Centro Estudios Moleculares de la Célula (CEMC), Departamento Bioquímica y Biología Molecular, Facultad Ciencias Químicas y Farmacéuticas, Universidad de Chile, Santiago, Chile; Division of Cardiology, Department of Medicine, Emory University, Atlanta, GA, United States.
Pablo E MoralesAdvanced Center for Chronic Diseases (ACCDiS), Centro Estudios Moleculares de la Célula (CEMC), Departamento Bioquímica y Biología Molecular, Facultad Ciencias Químicas y Farmacéuticas, Universidad de Chile, Santiago, Chile.
Marina García-MiguelAdvanced Center for Chronic Diseases (ACCDiS), Centro Estudios Moleculares de la Célula (CEMC), Departamento Bioquímica y Biología Molecular, Facultad Ciencias Químicas y Farmacéuticas, Universidad de Chile, Santiago, Chile.
Ignacio Norambuena-SotoAdvanced Center for Chronic Diseases (ACCDiS), Centro Estudios Moleculares de la Célula (CEMC), Departamento Bioquímica y Biología Molecular, Facultad Ciencias Químicas y Farmacéuticas, Universidad de Chile, Santiago, Chile.
Benjamín Cartes-SaavedraAdvanced Center for Chronic Diseases (ACCDiS), Centro Estudios Moleculares de la Célula (CEMC), Departamento Bioquímica y Biología Molecular, Facultad Ciencias Químicas y Farmacéuticas, Universidad de Chile, Santiago, Chile.
Gonzalo Vidal-PeñaAdvanced Center for Chronic Diseases (ACCDiS), Centro Estudios Moleculares de la Célula (CEMC), Departamento Bioquímica y Biología Molecular, Facultad Ciencias Químicas y Farmacéuticas, Universidad de Chile, Santiago, Chile.
David Moncada-RuffAdvanced Center for Chronic Diseases (ACCDiS), Centro Estudios Moleculares de la Célula (CEMC), Departamento Bioquímica y Biología Molecular, Facultad Ciencias Químicas y Farmacéuticas, Universidad de Chile, Santiago, Chile.
Fernanda Sanhueza-OlivaresAdvanced Center for Chronic Diseases (ACCDiS), Centro Estudios Moleculares de la Célula (CEMC), Departamento Bioquímica y Biología Molecular, Facultad Ciencias Químicas y Farmacéuticas, Universidad de Chile, Santiago, Chile.
Alejandra San MartínDivision of Cardiology, Department of Medicine, Emory University, Atlanta, GA, United States.
Mario ChiongAdvanced Center for Chronic Diseases (ACCDiS), Centro Estudios Moleculares de la Célula (CEMC), Departamento Bioquímica y Biología Molecular, Facultad Ciencias Químicas y Farmacéuticas, Universidad de Chile, Santiago, Chile. Electronic address: mchiong@uchile.cl.
Advanced Center for Chronic Diseases · CLEmory University · US

Funding

T cell triggering events and hypertensionP01HL095070 · NHLBI · EMORY UNIVERSITY · PI JO, HANJOONG · 2009 to 2019
$20.5M
Mechanically Stressed VSMC: A Role for Slingshot Phosphatase in InflammationR01HL113167 · NHLBI · EMORY UNIVERSITY · PI SAN MARTIN, ALEJANDRA · 2013 to 2017
$1.9M
NHLBI NIH HHS HL113167NHLBI NIH HHS P01 HL095070NHLBI NIH HHS R01 HL113167
6 · The paper itself

Abstract

Glucagon-like peptide-1 (GLP-1) is a neuroendocrine hormone produced by gastrointestinal tract in response to food ingestion. GLP-1 plays a very important role in the glucose homeostasis by stimulating glucose-dependent insulin secretion, inhibiting glucagon secretion, inhibiting gastric emptying, reducing appetite and food intake. Because of these actions, the GLP-1 peptide-mimetic exenatide is one of the most promising new medicines for the treatment of type 2 diabetes. In vivo treatments with GLP-1 or exenatide prevent neo-intima layer formation in response to endothelial damage and atherosclerotic lesion formation in aortic tissue. Whether GLP-1 modulates vascular smooth muscle cell (VSMC) migration and proliferation by controlling mitochondrial dynamics is unknown. In this report, we showed that GLP-1 increased mitochondrial fusion and activity in a PKA-dependent manner in the VSMC cell line A7r5. GLP-1 induced a Ser-637 phosphorylation in the mitochondrial fission protein Drp1, and decreased Drp1 mitochondrial localization. GLP-1 inhibited PDGF-BB-induced VSMC migration and proliferation, actions inhibited by overexpressing wild type Drp1 and mimicked by the Drp1 inhibitor Mdivi-1 and by overexpressing dominant negative Drp1. These results show that GLP-1 stimulates mitochondrial fusion, increases mitochondrial activity and decreases PDGF-BB-induced VSMC dedifferentiation by a PKA/Drp1 signaling pathway. Our data suggest that GLP-1 inhibits vascular remodeling through a mitochondrial dynamics-dependent mechanism.

Indexed as

AnimalsBiomimetic MaterialsCell Culture TechniquesCell DedifferentiationCell LineCell MovementCell ProliferationEndothelial CellsGlucagon-Like Peptide 1Membrane Potential, MitochondrialMicroscopy, ConfocalMitochondrial DynamicsMitochondrial ProteinsMuscle, Smooth, VascularPeptide FragmentsRatsGlucagon-Like Peptide 1glucagon-like peptide 1 (7-36)amideMitochondrial ProteinsPeptide FragmentsDrp1GLP-1Mitochondrial dynamicsVSMCVSMC dedifferentiation

Identifiers

PMID26807480
PMCPMC4775317
OpenAlexW2274894148

What OpenQuestion holds

Textmetadata
LicenceTDM
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.