Evidence map›Paper›PMID 24276258›Full record

ArticlePharmaceuticals (Basel, Switzerland)2013

Dysregulation of the Mammalian Target of Rapamycin and p27Kip1 Promotes Intimal Hyperplasia in Diabetes Mellitus.

Thomas Cooper Woods

Open access · goldAbstract read
In one paragraph

Article in Pharmaceuticals (Basel, Switzerland), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

10 citing papers in PubMed, 19 citations in OpenAlex.

  1. Trial
  2. Clinical outcomes after permanent polymer or polymer-free stent implantation in patients with diabetes mellitus: The ReCre8 diabetes substudy.Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions · 2022
    Trial
  3. Three-year clinical outcomes of the absorb bioresorbable vascular scaffold compared to Xience everolimus-eluting stent in routine PCI in patients with diabetes mellitus-AIDA sub-study.Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions · 2021
    Trial
  4. Article
  5. Article
  6. Article
  7. PCI in Patients with Diabetes: Role of the Cre8 Drug-eluting Stent.Interventional cardiology (London, England) · 2017
    Article
  8. Review
  9. Article
  10. Overnutrition, mTOR signaling, and cardiovascular diseases.American journal of physiology. Regulatory, integrative and comparative physiology · 2014
    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

1 author at 1 institution in 1 country.

Thomas Cooper WoodsTulane Heart and Vascular Institute and the Department of Physiology, School of Medicine, Tulane University, 1430 Tulane Avenue, SL-48, New Orleans, LA 70112, USA. twoods3@tulane.edu.
Tulane University · US

Funding

VASCULAR SMOOTH MUSCLE PLASTICITY IN NITRIC OXIDEP20RR018766 · NCRR · LSU HEALTH SCIENCES CENTER · PI KAPUSTA, DANIEL R · 2003 to 2011
$18.5M
MENTORING IN CARDIOVASCULAR BIOLOGYP20GM103514 · NIGMS · LSU HEALTH SCIENCES CENTER · PI KAPUSTA, DANIEL R · 2012 to 2012
$2.0M
NCRR NIH HHS P20 RR018766NIGMS NIH HHS P20 GM103514
6 · The paper itself

Abstract

The proliferation and migration of vascular smooth muscle cells (VSMCs) in the intima of an artery, known as intimal hyperplasia, is an important component of cardiovascular diseases. This is seen most clearly in the case of in-stent restenosis, where drug eluting stents are used to deliver agents that prevent VSMC proliferation and migration. One class of agents that are highly effective in the prevention of in-stent restenosis is the mammalian Target of Rapamycin (mTOR) inhibitors. Inhibition of mTOR blocks protein synthesis, cell cycle progression, and cell migration. Key to the effects on cell cycle progression and cell migration is the inhibition of mTOR-mediated degradation of p27Kip1 protein. p27Kip1 is a cyclin dependent kinase inhibitor that is elevated in quiescent VSMCs and inhibits the G1 to S phase transition and cell migration. Under normal conditions, vascular injury promotes degradation of p27Kip1 protein in an mTOR dependent manner. Recent reports from our lab suggest that in the presence of diabetes mellitus, elevation of extracellular signal response kinase activity may promote decreased p27Kip1 mRNA and produce a relative resistance to mTOR inhibition. Here we review these findings and their relevance to designing treatments for cardiovascular disease in the presence of diabetes mellitus.

Identifiers

PMID24276258
PMCPMC3816729
OpenAlexW2148284122

What OpenQuestion holds

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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.