Evidence map›Paper›PMID 31571663›Full record

ArticleNeural regeneration research2020

The Schlager mouse as a model of altered retinal phenotype.

Lakshini Y Herat, Aaron L Magno, Márcio G Kiuchi, Kristy L Jackson, Revathy Carnagarin, Geoffrey A Head, Markus P Schlaich, Vance B Matthews

Open access · goldAbstract read
In one paragraph

Article in Neural regeneration research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

7 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Article
  3. Impact of Arterial Hypertension on the Eye: A Review of the Pathogenesis, Diagnostic Methods, and Treatment of Hypertensive Retinopathy.Medical science monitor : international medical journal of experimental and clinical research · 2022
    Review
  4. Article
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  6. Review
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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

8 authors at 3 institutions in 1 country.

Lakshini Y HeratDobney Hypertension Centre, School of Biomedical Science - Royal Perth Hospital Unit, University of Western Australia, Perth, Australia.
Aaron L MagnoResearch Centre, Royal Perth Hospital, Perth, Australia.
Márcio G KiuchiDobney Hypertension Centre, School of Medicine - Royal Perth Hospital Unit, University of Western Australia, Perth, Australia.
Kristy L JacksonNeuropharmacology Laboratory, Baker Heart and Diabetes Institute, Melbourne, Australia.
Revathy CarnagarinDobney Hypertension Centre, School of Medicine - Royal Perth Hospital Unit, University of Western Australia, Perth, Australia.
Geoffrey A HeadNeuropharmacology Laboratory, Baker Heart and Diabetes Institute, Melbourne, Australia.
Markus P SchlaichDobney Hypertension Centre, School of Medicine - Royal Perth Hospital Unit, University of Western Australia; Department of Cardiology and Department of Nephrology, Royal Perth Hospital, Perth, Australia.
Vance B MatthewsDobney Hypertension Centre, School of Biomedical Science - Royal Perth Hospital Unit, University of Western Australia, Perth, Australia.
Royal Perth Hospital · AUBaker Heart and Diabetes Institute · AUUniversity of Western Australia · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypertension is a risk factor for a large number of vision-threatening eye disorders. In this study, we investigated for the first time the retinal neural structure of the hypertensive BPH/2J mouse (Schlager mouse) and compared it to its control counterpart, the normotensive BPN/3J strain. The BPH/2J mouse is a selectively inbred mouse strain that develops chronic hypertension due to elevated sympathetic nervous system activity. When compared to the BPN/3J strain, the hypertensive BPH/2J mice showed a complete loss of outer layers of the neural retina at 21 weeks of age, which was indicative of a severe vision-threatening disease potentially caused by hypertension. To elucidate whether the retinal neural phenotype in the BPH/2J strain was attributed to increased BP, we investigated the neural retina of both BPN/3J and BPH/2J mice at 4 weeks of age. Our preliminary results showed for the first time that the BPH/2J strain develops severe retinal neural damage at a young age. Our findings suggest that the retinal phenotype in the BPH/2J mouse is possibly due to elevated blood pressure and may be contributed by an early onset spontaneous mutation which is yet to be identified or a congenital defect occurring in this strain. Further characterization of the BPH/2J mouse strain is likely to i) elucidate gene defects underlying retinal disease; ii) understand mechanisms leading to neural retinal disease and iii) permit testing of molecules for translational research to interfere with the progression of retinal disease. The animal experiments were performed with the approval of the Royal Perth Hospital Animal Ethics Committee (R535/17-18) on June 1, 2017.

Indexed as

blood pressureeyehypertensionmiceneural regenerationretinaSchlager mousesympathetic nervous system

Identifiers

PMID31571663
PMCPMC6921339
OpenAlexW2975611420

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.