ArticleInvestigative ophthalmology & visual science2013
Modulation of angiogenesis by genetic manipulation of ATF4 in mouse model of oxygen-induced retinopathy [corrected].
Article in Investigative ophthalmology & visual science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 17 papers.
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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.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- SLC7A11-mediated disulfidptosis underlies the pathogenesis of proliferative diabetic retinopathy.Eye and vision (London, England) · 2026Article
- Spatial transcriptomics reveals regionally altered gene expression that drives retinal degeneration.Communications biology · 2025Article
- The role of vitamin K and its antagonist in the process of ferroptosis-damaged RPE-mediated CNV.Cell death & disease · 2025Article
- The Involvement of Unfolded Protein Response in the Mechanism of Nitrogen Mustard-Induced Ocular Toxicity.The Journal of pharmacology and experimental therapeutics · 2024Article
- The endoplasmic reticulum: Homeostasis and crosstalk in retinal health and disease.Progress in retinal and eye research · 2024Review
- PERK Inhibition Suppresses Neovascularization and Protects Neurons During Ischemia-Induced Retinopathy.Investigative ophthalmology & visual science · 2023Article
- Integrated Stress Response Regulation of Corneal Epithelial Cell Motility and Cytokine Production.Investigative ophthalmology & visual science · 2022Article
- Diabetic Retinopathy: From Animal Models to Cellular Signaling.International journal of molecular sciences · 2022Review
- Role of Activating Transcription Factor 4 in Murine Choroidal Neovascularization Model.International journal of molecular sciences · 2021Article
- Article
- Endoplasmic reticulum stress: New insights into the pathogenesis and treatment of retinal degenerative diseases.Progress in retinal and eye research · 2020Review
- Neurodegeneration: Keeping ATF4 on a Tight Leash.Frontiers in cellular neuroscience · 2017Review
- Article
- Activated complement classical pathway in a murine model of oxygen-induced retinopathy.International journal of ophthalmology · 2015Article
- Article
- Increased ER stress as a mechanism of retinal neurovasculopathy in mice with severe hyperhomocysteinemia.Austin journal of clinical ophthalmology · 2014Article
- Review: retinal degeneration: focus on the unfolded protein response.Molecular vision · 2013Review
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
purposeThe activation of the unfolded protein response (UPR) and an increase in activating transcription factor 4 (ATF4) has been previously reported in the diabetic retina. Despite this, a direct link between ATF4 and the degree of proliferative retinopathy has not been demonstrated to date. Therefore, the objective of this study was to determine whether ATF4 deficiency could reduce neovascularization in mice with oxygen-induced retinopathy (OIR).
methodsWe induced OIR in C57BL/6, ATF4(+/-), and endoplasmic reticulum stress-activated indicator (ERAI) mice and used quantitative RT-PCR and Western blot analysis to evaluate relative gene and protein expression. Histology and microscopy were used to calculate the extent of neovascularization in flat-mounted retinas.
resultsExperimental data revealed Xbp1 splicing in the retinal ganglia cells, outer plexiform layer, inner nuclear layer, and outer nuclear layer and in pericytes of postdevelopment day 17 ERAI OIR mice, confirming the activation of IRE1 UPR signaling. In naive ATF4-deficient mice, we also observed an elevation in UPR-associated and vascular-associated gene expression (Bip, Atf6, Hif1a, Pik3/Akt, Flt1/Vegfa, and Tgfb1), which may have contributed to the alleviation of hypoxia-driven neovascularization in experimental ATF4(+/-) retinas. The OIR ATF4(+/-) retinas demonstrated reprogramming of the UPR seen at both the mRNA (Atf6 and Bip) and protein (pATF6 and peIf2α) levels, as well as a reduction in vascularization-associated gene expression (Flt1, Vegf1, Hif1, and Tgb1). These changes corresponded to the decline in the rate of neovascularization.
conclusionsOur study validates ATF4 as a prospective therapeutic target to inhibit neovascularization in proliferative retinopathy.
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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.