Evidence map›Paper›PMID 16894343›Full record

ArticleBritish journal of pharmacology2006

Rapamycin induces regression of endometriotic lesions by inhibiting neovascularization and cell proliferation.

M W Laschke, A Elitzsch, C Scheuer, J H Holstein, B Vollmar, M D Menger

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
7.6field-weighted citation impact, top 3% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Effect of rapamycin on endometriosis in mice.Experimental and therapeutic medicine · 2016
    Article
  11. Article
  12. Angiogenesis and endometriosis.Obstetrics and gynecology international · 2013
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Inhibition of the mTORC1 pathway suppresses intestinal polyp formation and reduces mortality in ApcDelta716 mice.Proceedings of the National Academy of Sciences of the United States of America · 2008
    Article
  19. Rapamycin affects early fracture healing in mice.British journal of pharmacology · 2008
    Article
  20. PTEN loss does not predict for response to RAD001 (Everolimus) in a glioblastoma orthotopic xenograft test panel.Clinical cancer research : an official journal of the American Association for Cancer Research · 2008
    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

6 authors at 2 institutions in 1 country.

M W LaschkeInstitute for Clinical and Experimental Surgery, University of Saarland, Homburg/Saar, Germany. matthias.laschke@uniklinik-saarland.de
A Elitzsch
C Scheuer
J H Holstein
B Vollmar
M D Menger
Saarland University · DEUniversity of Rostock · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeRapamycin is a widely used drug with antifungal, immunosuppressant and antiangiogenic effects. Herein, we studied whether immunosuppressive doses of rapamycin are capable of influencing endometriotic lesions. EXPERIMENTAL APPROACH: We tested in vitro the potential of rapamycin to inhibit endothelial cell sprouting using the aortic ring assay and we further studied its effect on the expression of proliferating cell nuclear antigen (PCNA), apoptotic cell death-associated activated caspase-3 and vascular endothelial growth factor (VEGF) in cultured endometrial tissue fragments. In addition, we analyzed the drug in vivo after induction of endometriotic lesions by transplanting isolated endometrial fragments into the dorsal skinfold chamber of Syrian golden hamsters. Using intravital fluorescence microscopy, we repetitively analyzed angiogenesis, neovascularization and microcirculatory parameters over a time period of 14 days in rapamycin-treated animals and DMSO-treated controls. KEY

resultsAdministration of rapamycin significantly reduced the size of the endometriotic lesions. This was associated by inhibition of VEGF-mediated angiogenesis as indicated by a suppression of endothelial cell sprouting in vitro and a reduction of microvessel density in endometriotic lesions in vivo. Moreover, rapamycin directly inhibited cell proliferation within endometrial tissue, while manifestation of apoptotic cell death remained unaffected. CONCLUSIONS AND IMPLICATIONS: Our data indicate that administration of rapamycin may represent a novel therapeutic approach for an antiangiogenic treatment of endometriosis.

Indexed as

AnimalsAortaCell ProliferationCricetinaeEndometriosisFemaleImmunosuppressive AgentsMesocricetusMicroscopy, FluorescenceNeovascularization, PathologicSirolimusImmunosuppressive AgentsSirolimus

Identifiers

PMID16894343
PMCPMC2013796
OpenAlexW1613230448

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.