ArticlePloS one2015
Attenuation of choroidal neovascularization by histone deacetylase inhibitor.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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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.
The trial behind it
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Macrophage metabolic reprogramming via HIF-1α-glycolysis drives osteoblast ferroptosis and bone loss through an IL-6-STAT3-dependent redox axis.Redox report : communications in free radical research · 2026Article
- Age-Related Macular Degeneration: Cellular and Molecular Signaling Mechanisms.International journal of molecular sciences · 2025Review
- Protein Acetylation in Age-Related Macular Degeneration: Mechanisms, Roles, and Therapeutic Perspectives.Investigative ophthalmology & visual science · 2025Review
- The essential role of N6-methyladenosine RNA methylation in complex eye diseases.Genes & diseases · 2023Review
- Oxidative stress and epigenetics in ocular vascular aging: an updated review.Molecular medicine (Cambridge, Mass.) · 2023Review
- NURR1 expression regulates retinal pigment epithelial-mesenchymal transition and age-related macular degeneration phenotypes.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Anti-VEGF Drugs Influence Epigenetic Regulation and AMD-Specific Molecular Markers in ARPE-19 Cells.Cells · 2021Article
- Inhibition of laser induced rats choroidal neovascularization by intravitreous injection of sEphB4-HSA.Annals of translational medicine · 2021Article
- An Updated Review of the Epigenetic Mechanism Underlying the Pathogenesis of Age-related Macular Degeneration.Aging and disease · 2020Review
- RPE epithelial-mesenchymal transition plays a critical role in the pathogenesis of proliferative vitreoretinopathy.Annals of translational medicine · 2020Article
- The Histone Deacetylase Inhibitor AN7, Attenuates Choroidal Neovascularization in a Mouse Model.International journal of molecular sciences · 2019Article
- Epigenetic control of gene regulation during development and disease: A view from the retina.Progress in retinal and eye research · 2018Review
- Pathogenic role and therapeutic potential of pleiotrophin in mouse models of ocular vascular disease.Angiogenesis · 2017Article
- Targeting the ROS-HIF-1-endothelin axis as a therapeutic approach for the treatment of obstructive sleep apnea-related cardiovascular complications.Pharmacology & therapeutics · 2016Review
- Histone Deacetylase Inhibition Restores Retinal Pigment Epithelium Function in Hyperglycemia.PloS one · 2016Article
- The regulatory role of hepatoma-derived growth factor as an angiogenic factor in the eye.Molecular vision · 2016Article
- Inhibition of HDAC1 and 3 in the Presence of Systemic Inflammation Reduces Retinal Degeneration in a Model of Dry Age-Related Macular Degeneration.Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and TherapeuticsArticle
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Choroidal neovascularization (CNV) is a blinding complication of age-related macular degeneration that manifests as the growth of immature choroidal blood vessels through Bruch's membrane, where they can leak fluid or hemorrhage under the retina. Here, we demonstrate that the histone deacetylase inhibitor (HDACi) trichostatin A (TSA) can down-regulate the pro-angiogenic hypoxia-inducible factor-1α and vascular endothelial growth factor (VEGF), and up-regulate the anti-angiogenic and neuro-protective pigment epithelium derived factor in human retinal pigment epithelial (RPE) cells. Most strikingly, TSA markedly down-regulates the expression of VEGF receptor-2 in human vascular endothelial cells and, thus, can knock down pro-angiogenic cell signaling. Additionally, TSA suppresses CNV-associated wound healing response and RPE epithelial-mesenchymal transdifferentiation. In the laser-induced model of CNV using C57Bl/6 mice, systemic administration of TSA significantly reduces fluorescein leakage and the size of CNV lesions at post-laser days 7 and 14 as well as the immunohistochemical expression of VEGF, VEGFR2, and smooth muscle actin in CNV lesions at post-laser day 7. This report suggests that TSA, and possibly HDACi's in general, should be further evaluated for their therapeutic potential for the treatment of CNV.
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Registered trials
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.