Evidence mapPaperPMID 32093902Full record

ArticleThe American journal of pathology2020

Erythropoietin Receptor Signaling Supports Retinal Function after Vascular Injury.

Colin A Bretz, Aaron B Simmons, Eric Kunz, Aniket Ramshekar, Carson Kennedy, Ivan Cardenas, M Elizabeth Hartnett

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

15 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Pathophysiology of Retinopathy of Prematurity.Annual review of vision science · 2023
    Review
  6. Systemic Cytokines in Retinopathy of Prematurity.Journal of personalized medicine · 2023
    Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. 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

7 authors at 1 institution in 1 country.

Colin A BretzJohn A. Moran Eye Center, University of Utah, Salt Lake City, Utah.
Aaron B SimmonsJohn A. Moran Eye Center, University of Utah, Salt Lake City, Utah.
Eric KunzJohn A. Moran Eye Center, University of Utah, Salt Lake City, Utah.
Aniket RamshekarJohn A. Moran Eye Center, University of Utah, Salt Lake City, Utah.
Carson KennedyJohn A. Moran Eye Center, University of Utah, Salt Lake City, Utah.
Ivan CardenasJohn A. Moran Eye Center, University of Utah, Salt Lake City, Utah.
M Elizabeth HartnettJohn A. Moran Eye Center, University of Utah, Salt Lake City, Utah. Electronic address: me.hartnett@hsc.utah.edu.
University of Utah · US

Funding

University of Utah Core Vision Research GrantP30EY014800 · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · 2005 to 2025
$1.4M
Mechanisms of Angiogenesis in ROPR01EY015130 · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · 2005 to 2025
$660k
Endothelial Transmigration in Neovascular Age-related Macular DegenerationR01EY017011 · STANFORD UNIVERSITY · 2025 to 2025
$451k
NEI NIH HHS P30 EY014800NEI NIH HHS R01 EY015130NEI NIH HHS R01 EY017011
6 · The paper itself

Abstract

The investigation of erythropoietin (EPO) has expanded to include potential nonhematopoietic roles in neural and retinal diseases, including diabetic retinopathy. However, it remains unclear how EPO functions to support the neural retina. Transgenic mice with hypoactive EPO receptor (EPOR) signaling (hWtEPOR) were compared with littermate control mice (WT) to test the role of EPOR signaling under normal conditions and after vascular injury and regrowth into the retina. Although retinal function tested with OptoMotry and electroretinography was comparable to adult (8-week-old) littermate WT mice, hWtEPOR mice had thinner inner and outer plexiform layers and a greater number of amacrine cells. Injury and repair caused by the oxygen-induced retinopathy model reduced visual acuity thresholds, reduced electroretinography amplitudes, and thinned the outer plexiform and inner nuclear layers of both WT and hWtEPOR 8-week-old mice. In hWtEPOR compared with WT mice, scotopic a-wave amplitudes were reduced by injury, despite no change in outer nuclear layer thickness; and peripheral rod, but not cone number, was reduced. Scotopic b-waves were reduced in injured hWtEPOR mice compared with WT, and rod bipolar cell ectopic neurites were increased in both genotypes after injury, suggesting a potential reparative process to preserve connectivity and the b-wave. Normal EPOR signaling appeared important because ectopic neurites and b-waves were lower in the hWtEPOR than WT injured mice.

Indexed as

Signal TransductionAnimalsDiabetic RetinopathyElectroretinographyErythropoietinFemaleMaleMiceMice, TransgenicReceptors, ErythropoietinRetinaRetinal DiseasesVascular System InjuriesEpo protein, mouseErythropoietinReceptors, Erythropoietin

Identifiers

PMID32093902
PMCPMC7068470
OpenAlexW3007581677

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.