Evidence map›Paper›PMID 31621585›Full record

ArticleeLife2019

Targeting the vascular-specific phosphatase PTPRB protects against retinal ganglion cell loss in a pre-clinical model of glaucoma.

Benjamin R Thomson, Isabel A Carota, Tomokazu Souma, Saily Soman, Dietmar Vestweber, Susan E Quaggin

Open access · goldAbstract read
In one paragraph

Article in eLife, 2019. 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
4.6field-weighted citation impact, top 5% 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, 83 citations in OpenAlex.

  1. Pooled it
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  11. Penile cavernous sinusoids are Prox1-positive hybrid vessels.Vascular biology (Bristol, England) · 2024
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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

6 authors at 2 institutions in 2 countries.

Benjamin R ThomsonFeinberg Cardiovascular and Renal Research Institute, Northwestern University Feinberg School of Medicine, Chicago, United States.ORCID 0000-0001-6565-5866
Isabel A CarotaFeinberg Cardiovascular and Renal Research Institute, Northwestern University Feinberg School of Medicine, Chicago, United States.ORCID 0000-0002-7980-2377
Tomokazu SoumaFeinberg Cardiovascular and Renal Research Institute, Northwestern University Feinberg School of Medicine, Chicago, United States.ORCID 0000-0002-3285-8613
Saily SomanFeinberg Cardiovascular and Renal Research Institute, Northwestern University Feinberg School of Medicine, Chicago, United States.
Dietmar VestweberMax Planck Institute for Molecular Biomedicine, Münster, Germany.ORCID 0000-0002-3517-732X
Susan E QuagginFeinberg Cardiovascular and Renal Research Institute, Northwestern University Feinberg School of Medicine, Chicago, United States.ORCID 0000-0002-3706-5727
Northwestern University · USMax Planck Institute for Molecular Biomedicine · DE

Funding

Tumor Environment and Metastasis (TEAM) Research ProgramP30CA060553 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Daniela E Matei · 1993 to 2026
$153.9M
Renal Genomics CoreP30DK096493 · NIDDK · DUKE UNIVERSITY · PI COFFMAN, THOMAS M · 2012 to 2016
$5.9M
Activation of the Angiopoietin-Tie2/TEK Pathway to Treat Ocular Hypertension and GlaucomaR01EY025799 · NEI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI JIN, JING, QUAGGIN, SUSAN E. · 2016 to 2024
$5.8M
Therapeutics Development Core (Core B)P30DK114857 · NIDDK · NORTHWESTERN UNIVERSITY AT CHICAGO · PI SCHNAPER, H WILLIAM · 2018 to 2022
$5.7M
Exploiting Tie2 Activation for the Treatment of Vascular DiseasesR01HL124120 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI QUAGGIN, SUSAN E. · 2014 to 2017
$1.5M
NCI NIH HHS P30 CA060553NEI NIH HHS R01 EY025799NHLBI NIH HHS R01 HL124120NIDDK NIH HHS P30 DK096493NIDDK NIH HHS P30 DK114857NIH HHS P30 DK114857NIH HHS R01 EY025799NIH HHS R01 HL124120
6 · The paper itself

Abstract

Elevated intraocular pressure (IOP) due to insufficient aqueous humor outflow through the trabecular meshwork and Schlemm's canal (SC) is the most important risk factor for glaucoma, a leading cause of blindness worldwide. We previously reported loss of function mutations in the receptor tyrosine kinase TEK or its ligand ANGPT1 cause primary congenital glaucoma in humans and mice due to failure of SC development. Here, we describe a novel approach to enhance canal formation in these animals by deleting a single allele of the gene encoding the phosphatase PTPRB during development. Compared to

Indexed as

Gene Expression Regulation, DevelopmentalAllelesAngiopoietin-1AnimalsAqueous HumorCell CountDisease Models, AnimalGene DeletionGlaucomaHeterozygoteHumansIntraocular PressureMiceMice, KnockoutPhosphorylationReceptor-Like Protein Tyrosine Phosphatases, Class 3Angiopoietin-1Angpt1 protein, mousePtprb protein, mouseReceptor-Like Protein Tyrosine Phosphatases, Class 3Receptor, TIE-2Tek protein, mouseangiopoietindevelopmental biologyendotheliumglaucomahuman biologymedicinemousePTPRBSchlemm's canalTEKTie2VE-PTP

Identifiers

PMID31621585
PMCPMC6874417
OpenAlexW2980704889

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.