Evidence map›Paper›PMID 42228470›Full record

ArticleJCI insight2026

Characterization of vascular tortuosity throughout the murine oxygen-induced retinopathy model of ischemic retinopathy.

Kyle V Marra, Tomoya Murakami, Jimmy S Chen, Edith Aguilar, Jacob Robinson, Maxwell Prenner, Richard Daneman, Martin Friedlander, Eric Nudleman

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in JCI insight, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

9 authors.

Kyle V MarraShiley Eye Institute, Department of Ophthalmology, University of California, San Diego, San Diego, California, USA.
Tomoya MurakamiShiley Eye Institute, Department of Ophthalmology, University of California, San Diego, San Diego, California, USA.
Jimmy S ChenShiley Eye Institute, Department of Ophthalmology, University of California, San Diego, San Diego, California, USA.
Edith AguilarLowy Medical Research Institute, La Jolla, California, USA.
Jacob RobinsonLowy Medical Research Institute, La Jolla, California, USA.
Maxwell PrennerShiley Eye Institute, Department of Ophthalmology, University of California, San Diego, San Diego, California, USA.
Richard DanemanDepartment of Pharmacology and Neurosciences, University of California, San Diego, La Jolla, California, USA.
Martin FriedlanderLowy Medical Research Institute, La Jolla, California, USA.
Eric NudlemanShiley Eye Institute, Department of Ophthalmology, University of California, San Diego, San Diego, California, USA.

Funding

Cellular and Molecular Mechanisms of Retinal FibrosisR56EY032513 · NEI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI NUDLEMAN, ERIC D · 2023 to 2023
$427k
NEI NIH HHS R56 EY032513
6 · The paper itself

Abstract

Vascular tortuosity (VT) is a critical biomarker of disease progression that informs the decision to treat ischemic retinal disorders, particularly retinopathy of prematurity (ROP). The murine oxygen-induced retinopathy (OIR) model is the most widely used model of ischemic retinopathy. Although VT has been described in OIR, its temporal dynamics have not been systematically defined. In this study, a semiautomated artificial intelligence-based (AI-based) pipeline was used to quantify VT throughout OIR. Retinal flat mounts from age-matched normoxic and OIR mice (P10-P56) underwent vessel segmentation using a generative adversarial network (GAN), and VT was quantified as a cumulative tortuosity index with the iROP-Assist algorithm. Concurrently, standard OIR outcomes of neovascularization (NV) and vaso-obliteration (VO) were quantified using the algorithm at http://oirseg.org/. NV peaked at P17 and resolved by P23, while VO regressed over a similar interval. VT peaked with NV at P17 but remained elevated through P56. These temporal changes mirror both the development of VT and its persistence after NV regression observed clinically in ROP. Collectively, these findings establish VT as a durable, quantifiable phenotype in OIR and expand the model's utility beyond neovascular endpoints, providing a translational platform for investigating VT pathogenesis and evaluating the effects of therapeutic agents on VT.

Indexed as

IschemiaOxygenRetinal NeovascularizationRetinal VesselsRetinopathy of PrematurityAlgorithmsAnimalsDisease Models, AnimalDisease ProgressionFemaleGenerative Adversarial NetworksMiceMice, Inbred C57BLOxygenBiomarkersMouse modelsOphthalmologyRetinopathyVascular biology

Identifiers

PMID42228470
PMCPMC13461169

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.