Evidence map›Paper›PMID 32431177›Full record

ReviewFuture medicinal chemistry2020

Advances in mammalian target of rapamycin kinase inhibitors: application to devices used in the treatment of coronary artery disease.

Hiroyuki Jinnouchi, Liang Guo, Atsushi Sakamoto, Yu Sato, Anne Cornelissen, Rika Kawakami, Masayuki Mori, Sho Torii, Salome Kuntz, Emanuel Harari and 10 more

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Future medicinal chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 1 pooled it
0.2field-weighted citation impact, top 51% 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

4 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. 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

20 authors at 1 institution in 1 country.

Hiroyuki JinnouchiCardiovascular Department, CVPath Institute, Gaithersburg, MD 20878, USA.
Liang GuoCardiovascular Department, CVPath Institute, Gaithersburg, MD 20878, USA.
Atsushi SakamotoCardiovascular Department, CVPath Institute, Gaithersburg, MD 20878, USA.
Yu SatoCardiovascular Department, CVPath Institute, Gaithersburg, MD 20878, USA.
Anne CornelissenCardiovascular Department, CVPath Institute, Gaithersburg, MD 20878, USA.
Rika KawakamiCardiovascular Department, CVPath Institute, Gaithersburg, MD 20878, USA.
Masayuki MoriCardiovascular Department, CVPath Institute, Gaithersburg, MD 20878, USA.
Sho ToriiCardiovascular Department, CVPath Institute, Gaithersburg, MD 20878, USA.
Salome KuntzCardiovascular Department, CVPath Institute, Gaithersburg, MD 20878, USA.
Emanuel HarariCardiovascular Department, CVPath Institute, Gaithersburg, MD 20878, USA.
Hiroyoshi MoriCardiovascular Department, CVPath Institute, Gaithersburg, MD 20878, USA.
Daniela FullerCardiovascular Department, CVPath Institute, Gaithersburg, MD 20878, USA.
Neel GadhokeCardiovascular Department, CVPath Institute, Gaithersburg, MD 20878, USA.
Raquel FernandezCardiovascular Department, CVPath Institute, Gaithersburg, MD 20878, USA.
Ka Hyun PaekCardiovascular Department, CVPath Institute, Gaithersburg, MD 20878, USA.
Dipti SurveCardiovascular Department, CVPath Institute, Gaithersburg, MD 20878, USA.
Maria RomeroCardiovascular Department, CVPath Institute, Gaithersburg, MD 20878, USA.
Frank D KolodgieCardiovascular Department, CVPath Institute, Gaithersburg, MD 20878, USA.
Renu VirmaniCardiovascular Department, CVPath Institute, Gaithersburg, MD 20878, USA.
Aloke V FinnCardiovascular Department, CVPath Institute, Gaithersburg, MD 20878, USA.
CVPath Institute · US

Funding

IL1beta signaling in SMCpromotes beneficial changes in late stage atherosclerotic lesion pathogenesisR01HL141425 · NHLBI · UNIVERSITY OF VIRGINIA · PI OWENS, GARY K · 2019 to 2022
$3.1M
NHLBI NIH HHS R01 HL141425
6 · The paper itself

Abstract

Mammalian target of rapamycin (mTOR) inhibitors have been applied to vascular coronary devices to avoid neointimal growth and have become the predominant pharmacological agents used to prevent restenosis. mTOR inhibitors can affect not only proliferating vascular smooth muscle cells but also endothelial cells and therefore can result in delayed healing of the vessel including endothelialization. Emerging evidence suggests accelerated atherosclerosis due to the downstream negative effects on endothelial barrier functional recovery. The development of neoatherosclerosis within the neointima of drug-eluting stents can result in late thrombotic events. This type of problematic healing response may open the way for specific mTOR kinase inhibitors, such as ATP-competitive mTOR inhibitors. These inhibitors demonstrate a better healing profile than traditional limus-based drug-eluting stent and their clinical efficacy remains unknown.

Indexed as

AnimalsAtherosclerosisCoronary Artery DiseaseHumansProtein Kinase InhibitorsTOR Serine-Threonine KinasesProtein Kinase InhibitorsTOR Serine-Threonine KinasesmTORtorinvascular device

Identifiers

PMID32431177
PMCPMC7333590
OpenAlexW3026510307

What OpenQuestion holds

Textmetadata
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.