ArticleScientific reports2017
TGF-β participates choroid neovascularization through Smad2/3-VEGF/TNF-α signaling in mice with Laser-induced wet age-related macular degeneration.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 78 citations in OpenAlex.
- A graph retrieval-augmented generation pipeline for systematic drug target discovery: validation and application to ocular neovascularization.Briefings in bioinformatics · 2026Article
- The role of STAT3-targeted therapy created with COLIVELIN in the cross-talk between IL6/JAK2/STAT3 and TGF-β/SMAD2/SMAD3 signaling in a hyperinflammation and ROS-induced in vitro AMD model and its effect on retinal apoptosis.International ophthalmology · 2026Article
- The effect of age on wound healing in the laser induced choroidal neovascularization model.Experimental eye research · 2026Article
- Endothelial TGFβ signaling modulates choroidal neovascularization severity via myeloid-endothelial cell interaction.Frontiers in immunology · 2026Article
- CRX is an intrinsic suppressor of epithelial‒mesenchymal transition in retinal pigment epithelial cells: a promising therapeutic avenue for subretinal fibrosis.Cell death & disease · 2025Article
- Cannabidiol inhibits TGF-β1-induced epithelial-mesenchymal transition in human conjunctival epithelial cells by interrupting TGF-β/Smad signaling.Scientific reports · 2025Article
- RAGE Is Essential for Subretinal Fibrosis in Laser-Induced Choroidal Neovascularization: Therapeutic Implications.Investigative ophthalmology & visual science · 2025Article
- Decoding tumor angiogenesis: pathways, mechanisms, and future directions in anti-cancer strategies.Biomarker research · 2025Review
- Klotho attenuates epithelial‑mesenchymal transition of retinal pigment epithelial cells in subretinal fibrosis by suppressing the ERK1/2 and Wnt/β‑catenin signaling pathways.International journal of molecular medicine · 2025Article
- Rac1 overexpression promotes Treg-derived cytokines to mediate choroidal neovascularization in wet age-related macular degeneration.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2025Article
- Exosomal noncoding RNA: A potential therapy for retinal vascular diseases.Molecular therapy. Nucleic acids · 2024Review
- Treatment of neovascular age-related macular degeneration with anti-vascular endothelial growth factor drugs: progress from mechanisms to clinical applications.Frontiers in medicine · 2024Review
- Translating genetic findings to epigenetics: identifying the mechanisms associated with aging after high-radiation exposure on earth and in space.Frontiers in public health · 2024Article
- Exploring the role of granzyme B in subretinal fibrosis of age-related macular degeneration.Frontiers in immunology · 2024Review
- Gene Expression Within a Human Choroidal Neovascular Membrane Using Spatial Transcriptomics.Investigative ophthalmology & visual science · 2023Article
- Beyond VEGF: Targeting Inflammation and Other Pathways for Treatment of Retinal Disease.The Journal of pharmacology and experimental therapeutics · 2023Review
- Mechanisms of Acquired Resistance to Anti-VEGF Therapy for Neovascular Eye Diseases.Investigative ophthalmology & visual science · 2023Review
- Emerging therapeutic strategies for unmet need in neovascular age-related macular degeneration.Journal of translational medicine · 2023Review
- PRMT5 is a therapeutic target in choroidal neovascularization.Scientific reports · 2023Article
- Choroidal Neovascular Membranes in Retinal and Choroidal Tumors: Origins, Mechanisms, and Effects.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Choroidal neovascularization(CNV) is the most severe complication in Age-related macular degeneration(AMD) and the most common cause of irreversible blindness in the elderly in developed world. The aim of this study was to identify the effect of transforming growth factor-β(TGF-β) and Smad2/3-VEGF/TNF-α signaling on CNV angiopoiesis, and to explore TGF-β inhibitors on the development of CNV in a CNV mouse model. Fundus fluorescein angiography(FFA) was used to evaluate the laser-induced CNV formation. The histology of CNV lesions stained with hematoxylin-eosin(HE) was obtained. The immunofluorescent staining was performed to determine TGF-β protein expression. The expressions of TGF-β, phosphorylated Smad2/3, VEGF and TNF-α were determined by using Western blot analysis. The CNV areas were analyzed by using fluorescein stain on RPE/choroid-sclera flat mounts. We found the levels of TGF-β protein expression increasingly reached the peak till 3rd week during the CNV development. The protein levels of VEGF and TNF-α also increased significantly in CNV mice, which were inhibited by a synthetic TGF-β inhibitor LY2157299 or a natural TGF-β inhibitor Decorin. The phosphorylated Smad2/3 levels increased significantly in CNV mice, but this response was profoundly suppressed by the TGF-β inhibitors. Here we have demonstrated that TGF-β/Smad signaling plays an important role in Laser-induced CNV formation through down-regulation of VEGF and TNF-α expressions, suggesting TGF-β inhibitors may provide an alternative to traditional methods in wet AMD treatment.
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