Evidence map›Paper›PMID 27905925›Full record

ArticleCardiovascular diabetology2016

Expression of insulin receptor (IR) A and B isoforms, IGF-IR, and IR/IGF-IR hybrid receptors in vascular smooth muscle cells and their role in cell migration in atherosclerosis.

N Beneit, C E Fernández-García, J L Martín-Ventura, L Perdomo, Ó Escribano, J B Michel, G García-Gómez, S Fernández, S Díaz-Castroverde, J Egido and 2 more

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in Cardiovascular diabetology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04710186 (The Influence of Androgen Receptor, Insulin Like Growth Factor 1 Receptor, and Insulin Receptor in Male Patients With Peripheral Artery Disease), which is not on this map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 8% 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.

NCT04710186 unknown statusnot on this mapstarted 2018, after this paper: background citation

The Influence of Androgen Receptor, Insulin Like Growth Factor 1 Receptor, and Insulin Receptor in Male Patients With Peripheral Artery Disease

TypeobservationalSponsorUniversity of CatanzaroRan2018 to 2021Enrolled30ConditionsAndrogen Receptor Abnormal, Insulin-Like Growth Factor I Deficiency, Insulin Receptor, Defect inArmsarterial reconstructive open surgery
3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Receptor Tyrosine Kinase: Still an Interesting Target to Inhibit the Proliferation of Vascular Smooth Muscle Cells.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2023
    Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. PAPP-A and the IGF system in atherosclerosis: what's up, what's down?American journal of physiology. Heart and circulatory physiology · 2019
    Review
  18. IGF-1 and cardiovascular disease.Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society · 2019
    Review
  19. Article
  20. Review
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

12 authors at 5 institutions in 2 countries.

N BeneitBiochemistry and Molecular Biology II Department, School of Pharmacy, Complutense University of Madrid, Plaza Ramón y Cajal s/n, 28040, Madrid, Spain.
C E Fernández-GarcíaVascular Research Lab, IIS-Fundación Jiménez Diaz-Autonoma University, Madrid, Spain.
J L Martín-VenturaVascular Research Lab, IIS-Fundación Jiménez Diaz-Autonoma University, Madrid, Spain.
L PerdomoBiochemistry and Molecular Biology II Department, School of Pharmacy, Complutense University of Madrid, Plaza Ramón y Cajal s/n, 28040, Madrid, Spain.
Ó EscribanoBiochemistry and Molecular Biology II Department, School of Pharmacy, Complutense University of Madrid, Plaza Ramón y Cajal s/n, 28040, Madrid, Spain.
J B MichelInserm, U698, Universite Paris 7, CHU X-Bichat, Paris, France.
G García-GómezBiochemistry and Molecular Biology II Department, School of Pharmacy, Complutense University of Madrid, Plaza Ramón y Cajal s/n, 28040, Madrid, Spain.
S FernándezBiochemistry and Molecular Biology II Department, School of Pharmacy, Complutense University of Madrid, Plaza Ramón y Cajal s/n, 28040, Madrid, Spain.
S Díaz-CastroverdeBiochemistry and Molecular Biology II Department, School of Pharmacy, Complutense University of Madrid, Plaza Ramón y Cajal s/n, 28040, Madrid, Spain.
J EgidoCIBER of Diabetes and Associated Metabolic Diseases (CIBERDEM), Barcelona, Spain.
A Gómez-HernándezBiochemistry and Molecular Biology II Department, School of Pharmacy, Complutense University of Madrid, Plaza Ramón y Cajal s/n, 28040, Madrid, Spain. algomezh@ucm.es.
M BenitoBiochemistry and Molecular Biology II Department, School of Pharmacy, Complutense University of Madrid, Plaza Ramón y Cajal s/n, 28040, Madrid, Spain.
Universidad Complutense de Madrid · ESHospital Universitario Fundación Jiménez Díaz · ESCentro de Investigación Biomédica en Red Diabetes y Enfermedades Metabólicas Asociadas · ESInstituto de Investigación Sanitaria del Hospital Clínico San Carlos · ESUniversité Paris Cité · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAbnormal proliferation and migration of vascular smooth muscle cells (VSMCs) is a major contributor to the development of atherosclerotic process. In a previous work, we demonstrated that the insulin receptor isoform A (IRA) and its association with the insulin-like growth factor-I receptor (IGF-IR) confer a proliferative advantage to VSMCs. However, the role of IR and IGF-IR in VSMC migration remains poorly understood.

methodsWound healing assays were performed in VSMCs bearing IR (IRLoxP

resultsIGF-I strongly induced migration of the four cell lines through IGF-IR. In contrast, insulin and IGF-II only caused a significant increase of IRA VSMC migration which might be favored by the formation of IRA/IGF-IR receptors. Additionally, a specific IGF-IR inhibitor, picropodophyllin, completely abolished insulin- and IGF-II-induced migration in IRB, but not in IRA VSMCs. A significant increase of IRA and IGF-IR, and VSMC migration were observed in fibrous plaques from 24-week-old ApoE

conclusionsOur data suggest that overexpression of IGF-IR or IRA isoform, as homodimers or as part of IRA/IGF-IR hybrid receptors, confers a stronger migratory capability to VSMCs as might occur in early stages of atherosclerotic process.

Indexed as

Cell MovementReceptor Cross-TalkAnimalsAntigens, CDApolipoproteins EAtherosclerosisCell LineDiet, WesternDisease Models, AnimalGene Expression RegulationHumansInsulinInsulin-Like Growth Factor IInsulin-Like Growth Factor IIMaleMice, Inbred C57BLAntigens, CDApolipoproteins EIGF1R protein, humanINSR protein, humanInsulinInsulin-Like Growth Factor IInsulin-Like Growth Factor IIProtein IsoformsReceptor, IGF Type 1Receptor, InsulinReceptors, SomatomedinAtherosclerosisInsulin receptorMigrationVascular smooth muscle cells

Identifiers

PMID27905925
PMCPMC5134076
OpenAlexW2557943794

What OpenQuestion holds

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LicenceCC BY
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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.