Evidence map›Paper›PMID 25326112›Full record

ArticleDigestive diseases and sciences2014

Inhibition of endothelial Slit2/Robo1 signaling by thalidomide restrains angiogenesis by blocking the PI3K/Akt pathway.

Yinan Li, Sengwang Fu, Haiying Chen, Qian Feng, Yunjie Gao, Hanbing Xue, Zhizheng Ge, Jingyuan Fang, Shudong Xiao

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In one paragraph

Article in Digestive diseases and sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 24% 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

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

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Gefitinib-coated balloon inhibits the excessive hyperplasia of intima after vascular injuries through PI3K/AKT pathway.Technology and health care : official journal of the European Society for Engineering and Medicine · 2019
    Article
  9. Advances in the Medical Management of Vascular Anomalies.Seminars in interventional radiology · 2017
    Review
  10. Article
  11. Thalidomide-induced teratogenesis: history and mechanisms.Birth defects research. Part C, Embryo today : reviews · 2015
    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

9 authors at 3 institutions in 1 country.

Yinan LiShanghai Institution of Digestive Disease, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, 145 Middle Shandong Rd. GI Division, Shanghai, 200001, China.
Sengwang Fu
Haiying Chen
Qian Feng
Yunjie Gao
Hanbing Xue
Zhizheng Ge
Jingyuan Fang
Shudong Xiao
Renji Hospital · CNShanghai Jiao Tong University · CNState Key Laboratory of Oncogene and Related Genes · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThalidomide is effective in the treatment of angiodysplasia. The mechanisms underlying its activity may be associated with inhibition of angiogenic factors. It was recently shown that Slit2/Robo1 signaling plays a role in angiogenesis. PURPOSE: The aim of this study was to explore the expression and effects of Robo1 and Slit2 in angiodysplasia and to identify the possible therapeutic mechanisms of thalidomide.

methodSlit2 and Robo1 expression were analyzed in tissue samples and human umbilical vein endothelial cells (HUVECs) treated with thalidomide using a combination of laboratory assays that were able to detect functional activity.

resultsSlit2, Robo1 and vascular endothelial growth factor (VEGF) were strongly expressed in five angiodysplasia lesions out of seven cases, while expression was low in one out of seven normal tissues. Exposure of HUVECs to recombinant N-Slit2 resulted in an increase in VEGF levels and stimulated proliferation, migration and tube formation. These effects were blocked by an inhibitor of PI3K and thalidomide.

conclusionsRobo1 and Slit2 may have important roles in the formation of gastrointestinal vascular malformation. High concentrations of Slit2 increased the levels of VEGF in HUVECs via signaling through the PI3K/Akt pathway-an effect that could be inhibited by thalidomide.

Indexed as

Angiogenesis InhibitorsCells, CulturedChromonesEndothelial CellsGene Expression RegulationHumansIntercellular Signaling Peptides and ProteinsMorpholinesNeovascularization, PhysiologicNerve Tissue ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, ImmunologicRoundabout ProteinsSignal TransductionSlit Homolog 2 Protein2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneAngiogenesis InhibitorsChromonesIntercellular Signaling Peptides and ProteinsMorpholinesNerve Tissue ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, ImmunologicRoundabout ProteinsSlit Homolog 2 ProteinThalidomideVascular Endothelial Growth Factor A

Identifiers

PMID25326112
OpenAlexW2097094442

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.