ArticleEMBO molecular medicine2016
Increased VEGF-A promotes multiple distinct aging diseases of the eye through shared pathomechanisms.
Article in EMBO molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 51 citations in OpenAlex.
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- Topical Instillation of N-Acetylcysteine and N-Acetylcysteine Amide Impedes Age-Related Lens Opacity in Mice.Biomolecules · 2025Article
- Hypoxia-inducible factor-1 as targets for neuroprotection : from ferroptosis to Parkinson's disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Review
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- Anti-inflammatory potential of simvastatin and amfenac in ARPE-19 cells; insights in preventing re-detachment and proliferative vitreoretinopathy after rhegmatogenous retinal detachment surgery.International ophthalmology · 2024Article
- The role of NLRP3 inflammasome in aging and age-related diseases.Immunity & ageing : I & A · 2024Review
- Bioinformatics-based Study on the Effects of Umbilical Cord Mesenchymal Stem Cells on the Aging Retina.Current stem cell research & therapy · 2024Article
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- Atherosclerosis and Inflammation: Insights from the Theory of General Pathological Processes.International journal of molecular sciences · 2023Review
- SIRT1 Inhibits High Glucose-Induced TXNIP/NLRP3 Inflammasome Activation and Cataract Formation.Investigative ophthalmology & visual science · 2023Article
- The impact of early RPE cell junction loss on VEGF, Ang-2, and TIMP secretion in vitro.Molecular vision · 2023Article
- Early Post-ischemic Brain Glucose Metabolism Is Dependent on Function of TLR2: a Study Using [Molecular imaging and biology · 2022Article
- Crosstalk Between RPE Cells and Choroidal Endothelial Cells via the ANXA1/FPR2/SHP2/NLRP3 Inflammasome/Pyroptosis Axis Promotes Choroidal Neovascularization.Inflammation · 2022Article
- Intercellular communication analysis of the human retinal pigment epithelial and choroidal cells predicts pathways associated with aging, cellular senescence and age-related macular degeneration.Frontiers in aging neuroscience · 2022Article
- Common Genes Involved in Autophagy, Cellular Senescence and the Inflammatory Response in AMD and Drug Discovery Identified via Biomedical Databases.Translational vision science & technology · 2021Article
- Distinct effects of complement and of NLRP3- and non-NLRP3 inflammasomes for choroidal neovascularization.eLife · 2020Article
- NLRP3 inflammasome in endothelial dysfunction.Cell death & disease · 2020Review
- Ocular cytomegalovirus latency exacerbates the development of choroidal neovascularization.The Journal of pathology · 2020Article
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Authors and funding
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Funding
Abstract
While increased VEGF-A has been associated with neovascular age-related macular degeneration (AMD), it is not known whether VEGF-A may also promote other age-related eye diseases. Here, we show that an increase in VEGF-A is sufficient to cause multiple distinct common aging diseases of the eye, including cataracts and both neovascular and non-exudative AMD-like pathologies. In the lens, increased VEGF-A induces age-related opacifications that are associated with ERK hyperactivation, increased oxidative damage, and higher expression of the NLRP3 inflammasome effector cytokine IL-1β. Similarly, increased VEGF-A induces oxidative stress and IL-1β expression also in the retinal pigment epithelium (RPE). Targeting NLRP3 inflammasome components or Il1r1 strongly inhibited not only VEGF-A-induced cataract formation, but also both neovascular and non-exudative AMD-like pathologies. Moreover, increased VEGF-A expression specifically in the RPE was sufficient to cause choroidal neovascularization (CNV) as in neovascular AMD, which could be inhibited by RPE-specific inactivation of Flk1, while Tlr2 inactivation strongly reduced CNV. These findings suggest a shared pathogenic role of VEGF-A-induced and NLRP3 inflammasome-mediated IL-1β activation for multiple distinct ocular aging diseases.
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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.