Evidence map›Paper›PMID 23563308›Full record

ArticleThe Journal of clinical investigation2013

Endothelial SRF/MRTF ablation causes vascular disease phenotypes in murine retinae.

Christine Weinl, Heidemarie Riehle, Dongjeong Park, Christine Stritt, Susanne Beck, Gesine Huber, Hartwig Wolburg, Eric N Olson, Mathias W Seeliger, Ralf H Adams and 1 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

48 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
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  8. Transcription factors regulating vasculogenesis and angiogenesis.Developmental dynamics : an official publication of the American Association of Anatomists · 2024
    Review
  9. Article
  10. KnockdownBiomedicines · 2023
    Article
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  13. Review
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  19. Endothelial cell invasion is controlled by dactylopodia.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  20. 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

11 authors at 4 institutions in 4 countries.

Christine WeinlDepartment for Molecular Biology, Interfaculty Institute of Cell Biology, University of Tübingen, Tübingen, Germany.
Heidemarie Riehle
Dongjeong Park
Christine Stritt
Susanne Beck
Gesine Huber
Hartwig Wolburg
Eric N Olson
Mathias W Seeliger
Ralf H Adams
Alfred Nordheim
Institute of Cell Biology · UAPyrogenesis (Canada) · CAThe University of Texas Southwestern Medical Center · USUniversity of Tübingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Retinal vessel homeostasis ensures normal ocular functions. Consequently, retinal hypovascularization and neovascularization, causing a lack and an excess of vessels, respectively, are hallmarks of human retinal pathology. We provide evidence that EC-specific genetic ablation of either the transcription factor SRF or its cofactors MRTF-A and MRTF-B, but not the SRF cofactors ELK1 or ELK4, cause retinal hypovascularization in the postnatal mouse eye. Inducible, EC-specific deficiency of SRF or MRTF-A/MRTF-B during postnatal angiogenesis impaired endothelial tip cell filopodia protrusion, resulting in incomplete formation of the retinal primary vascular plexus, absence of the deep plexi, and persistence of hyaloid vessels. All of these features are typical of human hypovascularization-related vitreoretinopathies, such as familial exudative vitreoretinopathies including Norrie disease. In contrast, conditional EC deletion of Srf in adult murine vessels elicited intraretinal neovascularization that was reminiscent of the age-related human pathologies retinal angiomatous proliferation and macular telangiectasia. These results indicate that angiogenic homeostasis is ensured by differential stage-specific functions of SRF target gene products in the developing versus the mature retinal vasculature and suggest that the actin-directed MRTF-SRF signaling axis could serve as a therapeutic target in the treatment of human vascular retinal diseases.

Indexed as

AnimalsCell NucleusCytoplasmGene DeletionGene Expression RegulationMiceMice, KnockoutNeovascularization, PathologicNeovascularization, PhysiologicPhenotypeRetinaRetinal DiseasesRNA, MessengerSerum Response FactorTamoxifenTrans-ActivatorsMrtfa protein, mousemyocardin-related transcription factor B, mouseRNA, MessengerSerum Response FactorTamoxifenTrans-ActivatorsTranscription FactorsVascular Endothelial Growth Factor Avascular endothelial growth factor A, mouse

Identifiers

PMID23563308
PMCPMC3635718
OpenAlexW2155382351

What Socratic 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 Socratic graph.