Evidence map›Paper›PMID 28002872›Full record

ArticleClinical & experimental ophthalmology2017

Lutein facilitates physiological revascularization in a mouse model of retinopathy of prematurity.

Zhongjie Fu, Steven S Meng, Samuel B Burnim, Lois Eh Smith, Amy Cy Lo

Abstract read
In one paragraph

Article in Clinical & experimental ophthalmology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.9field-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

16 citing papers in PubMed, 25 citations in OpenAlex.

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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

5 authors at 2 institutions in 2 countries.

Zhongjie FuDepartment of Ophthalmology, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong.ORCID http://orcid.org/0000-0002-8182-2983
Steven S MengDepartment of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Samuel B BurnimDepartment of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Lois Eh SmithDepartment of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Amy Cy LoDepartment of Ophthalmology, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong.
Boston Children's Hospital · USUniversity of Hong Kong · HK

Funding

Dietary control of angiogenesis in retinopathy modelsR01EY017017 · NEI · BOSTON CHILDREN'S HOSPITAL · PI Zhongjie Fu, Lois Smith · 2006 to 2026
$11.8M
Novel therapies to inhibit Diabetic RetinopathyR24EY024864 · NEI · UNIVERSITY OF CALIFORNIA-IRVINE · PI KERN, TIMOTHY S · 2015 to 2019
$8.1M
Mouse Neurodevelopmental Behavior CoreU54HD090255 · NICHD · BOSTON CHILDREN'S HOSPITAL · PI KUNKEL, LOUIS M · 2016 to 2020
$5.2M
NEI NIH HHS R01 EY017017NEI NIH HHS R24 EY024864NICHD NIH HHS U54 HD090255
6 · The paper itself

Abstract

backgroundRetinopathy of prematurity is one of the leading causes of childhood blindness worldwide, with vessel growth cessation and vessel loss in phase I followed by neovascularization in phase II. Ischaemia contributes to its pathogenesis, and lutein protects against ischaemia-induced retinal damages. We aimed to investigate the effects of lutein on a murine model of oxygen-induced retinopathy.

methodsMouse pups were exposed to 75% oxygen for 5 days and returned to room air for another 5 days. Vascular obliteration, neovascularization and blood vessel leakage were examined. Immunohistochemistry for glial cells and microglia were performed.

resultsCompared with vehicle controls, mouse pups receiving lutein treatment displayed smaller central vaso-obliterated area and reduced blood vessel leakage. No significant difference in neovascular area was found between lutein and vehicle controls. Lutein promoted endothelial tip cell formation and maintained the astrocytic template in the avascular area in oxygen-induced retinopathy. No significant changes in Müller cell gliosis and microglial activation in the central avascular area were found in lutein-treated pups.

conclusionsOur observations indicated that lutein significantly promoted normal retinal vascular regrowth in the central avascular area, possibly through promoting endothelial tip cell formation and preserving astrocytic template. Our results indicated that lutein might be considered as a supplement for the treatment of proliferative retinopathy of prematurity because of its role in facilitating the revascularization of normal vasculature.

Indexed as

AnimalsAnimals, NewbornDisease Models, AnimalImmunohistochemistryLuteinMiceMice, Inbred C57BLNeovascularization, PathologicNeurogliaRetinal NeovascularizationRetinal VesselsRetinopathy of PrematurityLuteinoxygen-induced retinopathyretinopathy of prematurityvascular development

Identifiers

PMID28002872
PMCPMC5479763
OpenAlexW2564511414

What OpenQuestion holds

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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.