Evidence map›Paper›PMID 25499974›Full record

ArticleThe American journal of pathology2015

RhoA GTPase-induced ocular hypertension in a rodent model is associated with increased fibrogenic activity in the trabecular meshwork.

Padmanabhan P Pattabiraman, Tommy Rinkoski, Eric Poeschla, Alan Proia, Pratap Challa, Ponugoti V Rao

Open access · greenAbstract read
In one paragraph

Article in The American journal of pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
4.8field-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

37 citing papers in PubMed, 64 citations in OpenAlex.

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  10. Identification of the novel role of sterol regulatory element binding proteins (SREBPs) in mechanotransduction and intraocular pressure regulation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023
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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 1 country.

Padmanabhan P PattabiramanDepartment of Ophthalmology, Duke University School of Medicine, Durham, North Carolina.
Tommy RinkoskiDepartment of Molecular Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota.
Eric PoeschlaDepartment of Molecular Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota.
Alan ProiaDepartment of Pathology, Duke University School of Medicine, Durham, North Carolina.
Pratap ChallaDepartment of Ophthalmology, Duke University School of Medicine, Durham, North Carolina.
Ponugoti V RaoDepartment of Ophthalmology, Duke University School of Medicine, Durham, North Carolina; Department of Pharmacology and Cancer Biology, Duke University School of Medicine, Durham, North Carolina. Electronic address: p.rao@dm.duke.edu.
Duke University · USMayo Clinic · US

Funding

Trabecular Meshwork Cytoskeletal Signaling-Regulation of Aqueous Humor OutflowR01EY018590 · NEI · DUKE UNIVERSITY · PI RAO, P VASANTHA · 2008 to 2022
$5.6M
NEI NIH HHS R01 EY018590NEI NIH HHS R01EY18590
6 · The paper itself

Abstract

Ocular hypertension arising from increased resistance to aqueous humor (AH) outflow through the trabecular meshwork is a primary risk factor for open-angle glaucoma, a leading cause of blindness. Ongoing efforts have found little about the molecular and cellular bases of increased resistance to AH outflow through the trabecular meshwork in ocular hypertension patients. To test the hypothesis that dysregulated Rho GTPase signaling and a resulting fibrotic activity within the trabecular meshwork may result in ocular hypertension, we investigated the effects of expressing a constitutively active RhoA GTPase (RhoAV14) in the AH outflow pathway in Sprague-Dawley rats by using lentiviral vector-based gene delivery. Rats expressing RhoAV14 in the iridocorneal angle exhibited a significantly elevated intraocular pressure. Elevated intraocular pressure in the RhoAV14-expressing rats was associated with fibrotic trabecular meshwork and increased levels of F-actin, phosphorylated myosin light chain, α-smooth muscle actin, collagen-1A, and total collagen in the trabecular AH outflow pathway. Most of these changes were ameliorated by topical application of Rho kinase inhibitor. Human autopsy eyes from patients with glaucoma exhibited significant increases in levels of collagen-1A and total collagen in the trabecular AH outflow pathway. Collectively, these observations indicate that increased fibrogenic activity because of dysregulated RhoA GTPase activity in the trabecular AH outflow pathway increases intraocular pressure in a Rho kinase-dependent manner.

Indexed as

Mutation, MissenseAmino Acid SubstitutionAnimalsCollagenEye ProteinsFemaleHumansOcular HypertensionRatsRats, Sprague-DawleyrhoA GTP-Binding ProteinTrabecular MeshworkCollagenEye ProteinsrhoA GTP-Binding ProteinRHOA protein, human

Identifiers

PMID25499974
PMCPMC4305183
OpenAlexW2030668552

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.