Evidence map›Paper›PMID 42057040›Full record

ArticleJournal of translational medicine2026

Comprehensive multiomics analyses identify guanylate cyclase activator 1A as a photoreceptor-specific target in a murine model of oxygen-induced retinopathy.

Qianhui Yang, Jindan Wang, Tongrui Wu, Siyi Liu, Yumin Zhang, Xinglong Wang, Weiran Zhang, Hua Rong, Mengyu Wu, Yating Zhao and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

14 authors.

Qianhui Yang *Tianjin Key Laboratory of Retinal Functions and Diseases, Tianjin Branch of National Clinical Research Center for Ocular Disease, Eye Institute and School of Optometry, Tianjin Medical University Eye Hospital, Tianjin, 300384, China.
Jindan Wang *Tianjin Key Laboratory of Retinal Functions and Diseases, Tianjin Branch of National Clinical Research Center for Ocular Disease, Eye Institute and School of Optometry, Tianjin Medical University Eye Hospital, Tianjin, 300384, China.
Tongrui Wu *Songjiang Research Institute, Shanghai Key Laboratory of Emotions and Affective Disorders, Songjiang Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 201600, China.
Siyi Liu *Tianjin Key Laboratory of Retinal Functions and Diseases, Tianjin Branch of National Clinical Research Center for Ocular Disease, Eye Institute and School of Optometry, Tianjin Medical University Eye Hospital, Tianjin, 300384, China.
Yumin Zhang *Tianjin Key Laboratory of Retinal Functions and Diseases, Tianjin Branch of National Clinical Research Center for Ocular Disease, Eye Institute and School of Optometry, Tianjin Medical University Eye Hospital, Tianjin, 300384, China.
Xinglong WangTianjin Key Laboratory of Retinal Functions and Diseases, Tianjin Branch of National Clinical Research Center for Ocular Disease, Eye Institute and School of Optometry, Tianjin Medical University Eye Hospital, Tianjin, 300384, China.
Weiran ZhangTianjin Key Laboratory of Retinal Functions and Diseases, Tianjin Branch of National Clinical Research Center for Ocular Disease, Eye Institute and School of Optometry, Tianjin Medical University Eye Hospital, Tianjin, 300384, China.
Hua RongTianjin Key Laboratory of Retinal Functions and Diseases, Tianjin Branch of National Clinical Research Center for Ocular Disease, Eye Institute and School of Optometry, Tianjin Medical University Eye Hospital, Tianjin, 300384, China.
Mengyu WuHeart, Lung and Vessels Center, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, 610072, China.
Yating ZhaoHeart, Lung and Vessels Center, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, 610072, China.
Yunshan CaoHeart, Lung and Vessels Center, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, 610072, China.
Min ZhangClinical Research Center, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, 610072, China. sallyzhangmin@126.com.
Hui ShenLaboratory of Neurobiology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, 300070, China. shenhui@tmu.edu.cn.ORCID 0000-0002-8195-8143
Yan ZhangTianjin Key Laboratory of Retinal Functions and Diseases, Tianjin Branch of National Clinical Research Center for Ocular Disease, Eye Institute and School of Optometry, Tianjin Medical University Eye Hospital, Tianjin, 300384, China. yanzhang04@tmu.edu.cn.ORCID 0000-0003-2050-6343

Funding

Natural Science Foundation of Tianjin Municipality 25JCZDJC00090Open Project of Tianjin Key Laboratory of Retinal Functions and Diseases 2019tjswmq002the Tianjin Medical University Eye Hospital High-level Innovative Talent Program YDYYRCXM-E2023-06Tianjin High-level Talent Selection and Training Project in the Health Industry TJSJMYXYC-D2-042Tianjin Medical University Eye Hospital High-level Innovative Talent Program (YDYYRCXM-B2023-01), and the Tianjin Key Medical Discipline Construction Project YDYYRCXM-B2023-01
6 · The paper itself

Abstract

backgroundRetinopathy of prematurity (ROP), the leading cause of childhood blindness, is considered a vascular retinopathy; however, clinical studies have reported persistent electrophysiological dysfunctions in some ROP patients with remitted vasculopathy, resulting in severe visual impairments. Therefore, this study sought to unravel the mechanisms underlying persistent electrophysiological dysfunctions and identify a neuronal target in a murine model of oxygen-induced retinopathy (OIR), a widely used animal model for ROP.

methodsRetinal vascular morphology and leakage were examined by isolectin B4 staining and fluorescein fundus angiography in the OIR mouse model at P17 and P25. Full-field electroretinogram (ERG) was performed. Moreover, P17 retinas were analyzed with metabolomics and transcriptomics, and the results were validated by quantitative PCR (qPCR) and Western blotting (WB). Whole-cell patch clamp was used to evaluate phototransduction. Lentiviral particles carrying guanylate cyclase activator 1A (Guca1a) cDNA driven by a mouse rod opsin promoter were intravitreally injected into OIR mice, and immunofluorescence, ERG, patch clamp, cGMP measurement, and TUNEL staining were performed for assessments.

resultsVascular lesions in OIR retinas peaked at P17 and recovered at P25. However, a wave and b wave amplitudes in dark- and light-adapted ERGs under all light intensities were deficient at both developmental stages, and electrophysiological dysfunctions persisted in P32 OIR retinas. Multiomics indicates phototransduction defects in isolated photoreceptors. QPCR and WB validated the reduced Guca1a mRNA and its encoding protein levels in P17 and P25 OIR retinas. Patch clamp demonstrated impaired light responses of single rods. Furthermore, lentivirus-mediated photoreceptor-specific expression of GUCA1A recovered electrophysiological functions, improved single rod phototransduction, increased cGMP concentration, and reduced cell death in P17 and P25 OIR retinas.

conclusionsThe reduced GUCA1A in photoreceptors is mainly responsible for persistent electrophysiological dysfunctions in OIR mouse retinas, even after the recovery of vessel damage. The photoreceptor GUCA1A may serve as a neuronal target for ROP intervention.

Indexed as

Guanylate Cyclase-Activating ProteinsOxygenPhotoreceptor Cells, VertebrateRetinopathy of PrematurityAnimalsCyclic GMPDisease Models, AnimalElectroretinographyMiceMice, Inbred C57BLRetinaCyclic GMPGuanylate Cyclase-Activating ProteinsOxygenElectrophysiological dysfunctionGuanylate cyclase activator 1AGuca1a geneOxygen-induced retinopathy, retinopathy of prematurityPhototransduction

Identifiers

PMID42057040
PMCPMC13277265

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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.