Evidence map›Paper›PMID 1323129›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1992

Elimination of smooth muscle cells in experimental restenosis: targeting of fibroblast growth factor receptors.

W Casscells, D A Lappi, B B Olwin, C Wai, M Siegman, E H Speir, J Sasse, A Baird

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
12.2field-weighted citation impact, top 1% 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

27 citing papers in PubMed, 133 citations in OpenAlex.

  1. Article
  2. Fibroblast growth factor receptor 4 polymorphism is associated with increased risk and poor prognosis of non-Hodgkin's lymphoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Article
  3. Article
  4. Article
  5. Article
  6. Vascular smooth cell proliferation in perfusion culture of porcine carotid arteries.Biochemical and biophysical research communications · 2008
    Article
  7. Article
  8. Article
  9. Article
  10. The mechanisms of coronary restenosis: insights from experimental models.International journal of experimental pathology · 2000
    Review
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  12. Article
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  18. Review
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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

8 authors at 2 institutions in 1 country.

W CasscellsDepartment of Molecular and Cellular Growth Biology, Whittier Institute for Diabetes and Endocrinology, La Jolla, CA 92037.
D A Lappi
B B Olwin
C Wai
M Siegman
E H Speir
J Sasse
A Baird
Scripps Whittier Diabetes Institute · USShriners Hospitals for Children - Tampa · US

Funding

STUDIES WITH GROWTH HORMONE RELEASING FACTORP01DK018811 · NIDDK · WHITTIER INSTITUTE FOR DIABETES &ENDOC · PI MAHER, PAMELA ANNE · 1986 to 1995
–
NIDDK NIH HHS DK-18811
6 · The paper itself

Abstract

Factors in plasma and platelets do not fully account for the proliferation of smooth muscle cells in vascular injury, implying that additional factors are involved. Recently, we and others have observed that vascular injury regulates basic fibroblast growth factor, suggesting a further role for this pleiotropic factor. We report here that injury of rat arteries leads to an increase in fibroblast growth factor receptors in vascular smooth muscle cells. This up-regulation makes smooth muscle cells susceptible, in vitro and in vivo, to the lethal effects of a conjugate of basic fibroblast growth factor with the ribosome inactivator saporin. Saporin alone has no effect, whereas the conjugate kills proliferating, but not quiescent, smooth muscle cells in vitro. In vivo, one to three doses inhibit neointimal proliferation but have no apparent effect on the uninjured artery. Thus, the up-regulation of fibroblast growth factor receptors in vascular injury suggests new therapeutic possibilities for such refractory conditions as restenosis following balloon angioplasty.

Indexed as

ImmunotoxinsN-Glycosyl HydrolasesAmino Acid SequenceAngioplasty, BalloonAnimalsAntibodiesAortaArterial Occlusive DiseasesCell DivisionCells, CulturedDNA ReplicationFibroblast Growth Factor 2ImmunohistochemistryMaleMolecular Sequence DataMuscle, Smooth, VascularAntibodiesFibroblast Growth Factor 2ImmunotoxinsN-Glycosyl HydrolasesPeptidesPlant ProteinsReceptors, Cell SurfaceReceptors, Fibroblast Growth FactorRecombinant ProteinsRibosome Inactivating Proteins, Type 1Saporins

Identifiers

PMID1323129
PMCPMC49665
OpenAlexW2045272081

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.