Evidence map›Paper›PMID 18336244›Full record

ReviewCurrent drug targets2008

Intimal hyperplasia in murine models.

David Y Hui

Open access · greenAbstract readReview
In one paragraph

Review in Current drug targets, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

41 citing papers in PubMed, 79 citations in OpenAlex.

  1. Trial
  2. Review
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  9. Review
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  15. New Insights in the Pathophysiology of Antiphospholipid Syndrome.Seminars in thrombosis and hemostasis · 2018
    Review
  16. CaMKII (CaArteriosclerosis, thrombosis, and vascular biology · 2018
    Article
  17. Article
  18. Article
  19. Article
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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.

David Y HuiDepartment of Pathology and Laboratory Medicine, Genome Research Institute, University of Cincinnati College of Medicine, Cincinnati, Ohio 45237, USA. huidy@email.uc.edu
University of Cincinnati Medical Center · US

Funding

Role of Lipoprotein Receptors in Diet-induced Obesity and DiabetesR01DK074932 · NIDDK · UNIVERSITY OF CINCINNATI · PI HUI, DAVID YIU-KWAN · 2007 to 2019
$4.4M
APOLIPOPROTEIN E--IMPACT ON VASCULAR CELL FUNCTIONSR01HL061332 · NHLBI · UNIVERSITY OF CINCINNATI · PI HUI, DAVID Y · 1999 to 2006
$2.6M
NHLBI NIH HHS HL61332NHLBI NIH HHS R01 HL061332NIDDK NIH HHS R01 DK074932
6 · The paper itself

Abstract

The most commonly used procedures to induce arterial injury in mice are carotid artery ligation with cessation of blood flow and mechanically-induced denudation of endothelium in the carotid or the femoral arteries. Both procedures result in neointimal hyperplasia after two to three weeks. A survey of various inbred strains of mice shows that strain-specific differences in susceptibility to injury-induced neointimal hyperplasia are different than those for susceptibility to diet-induced atherosclerosis, with strains identified as susceptible to both neointimal hyperplasia and atherosclerosis, resistant to both, susceptible to atherosclerosis but resistant to neointimal hyperplasia, or resistant to atherosclerosis but susceptible to neointimal hyperplasia. Inflammatory cells such as T and B lymphocytes, which are contributory to atherosclerosis, are protective against injury-induced neointimal hyperplasia. In contrast, the infiltration of monocytes into the site of injury and their differentiation to macrophages favor neointimal hyperplasia similar to their pathogenic role in atherosclerosis. The regulatory role of lymphocytes and macrophages in neointimal hyperplasia is related to the production of cytokines such as interferon-gamma and tumor necrosis factor-alpha, respectively. Interestingly, inducible nitric oxide synthase (iNOS) activity appears to inhibit neointimal hyperplasia in the endothelial denudation model but contributes to neointimal hyperplasia when arterial injury is induced by periadventitial cuff placement. The difference appears to be due to the time required for endothelial recovery and the participation of inflammatory cells. Thus, although arterial injury-induced neointimal hyperplasia results in similar vascular occlusion as progressive atherosclerosis, the pathology and mechanism of the two disease processes are quite different.

Indexed as

Disease Models, AnimalAnimalsAtherosclerosisCarotid ArteriesFemoral ArteryHumansHyperplasiaLigationMiceTunica Intima

Identifiers

PMID18336244
PMCPMC2829189
OpenAlexW2089730495

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.