Evidence map›Paper›PMID 28851839›Full record

ArticleBioscience reports2017

Inhibition of p110δ PI3K prevents inflammatory response and restenosis after artery injury.

Antonio Bilancio, Barbara Rinaldi, Maria Antonietta Oliviero, Maria Donniacuo, Maria Gaia Monti, Amedeo Boscaino, Irene Marino, Lori Friedman, Francesco Rossi, Bart Vanhaesebroeck and 1 more

Open access · goldAbstract read
In one paragraph

Article in Bioscience reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 13% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Bindarit encapsulated nanoparticles prevent venous neointimal hyperplasia and restenosis in a murine angioplasty model.Translational research : the journal of laboratory and clinical medicine · 2022
    Article
  5. Article
  6. A Review of Phosphocreatine 3 Kinase δ Subtype (PI3Kδ) and Its Inhibitors in Malignancy.Medical science monitor : international medical journal of experimental and clinical research · 2021
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. 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

11 authors at 3 institutions in 1 country.

Antonio BilancioDepartment of Biochemistry, Biophysics and General Pathology, University of Campania "L. Vanvitelli", Naples, Italy antonio.bilancio@unicampania.it.
Barbara RinaldiDepartment of Experimental Medicine, Section of Pharmacology "L. Donatelli", University of Campania "L. Vanvitelli", Naples, Italy.
Maria Antonietta OlivieroDepartment of Biochemistry, Biophysics and General Pathology, University of Campania "L. Vanvitelli", Naples, Italy.
Maria DonniacuoDepartment of Experimental Medicine, Section of Pharmacology "L. Donatelli", University of Campania "L. Vanvitelli", Naples, Italy.
Maria Gaia MontiDepartment of Medical Translational Science, University of Naples "Federico II", Naples, Italy.
Amedeo BoscainoDepartment of Histopathology, AORN "Cardarelli", Naples, Italy.
Irene MarinoDepartment of Biochemistry, Biophysics and General Pathology, University of Campania "L. Vanvitelli", Naples, Italy.
Lori FriedmanTranslational Oncology, Genentech Inc, South San Francisco, CA, U.S.A.
Francesco RossiDepartment of Experimental Medicine, Section of Pharmacology "L. Donatelli", University of Campania "L. Vanvitelli", Naples, Italy.
Bart VanhaesebroeckCell Signalling, UCL Cancer Institute, Paul O'Gorman Building, University College London, 72 Huntley Street, London WC1E 6BT, U.K.
Antimo MigliaccioDepartment of Biochemistry, Biophysics and General Pathology, University of Campania "L. Vanvitelli", Naples, Italy.
University of Campania "Luigi Vanvitelli" · ITOspedale Antonio Cardarelli · ITUniversity of Naples Federico II · IT

Funding

Cancer Research UK 15965
6 · The paper itself

Abstract

Inflammatory cells play key roles in restenosis upon vascular surgical procedures such as bypass grafts, angioplasty and stent deployment but the molecular mechanisms by which these cells affect restenosis remain unclear. The p110δ isoform of phosphoinositide 3-kinase (PI3K) is mainly expressed in white blood cells. Here, we have investigated whether p110δ PI3K is involved in the pathogenesis of restenosis in a mouse model of carotid injury, which mimics the damage following arterial grafts. We used mice in which p110δ kinase activity has been disabled by a knockin (KI) point mutation in its ATP-binding site (p110δ

Indexed as

AnimalsCarotid ArteriesCarotid Artery InjuriesCarotid StenosisClass I Phosphatidylinositol 3-KinasesDisease Models, AnimalGene Knock-In TechniquesInflammationMaleMice, Inbred C57BLNeointimaPoint Mutation1-phosphatidylinositol 3-kinase p110 subunit, mouseClass I Phosphatidylinositol 3-Kinasescarotidinflammatory cellp110δPhosphoinositide 3-kinase (PI3K)restenosis

Identifiers

PMID28851839
PMCPMC5617917
OpenAlexW2753350383

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.