ArticleAngiogenesis2024
Granzyme B degrades extracellular matrix and promotes inflammation and choroidal neovascularization.
Article in Angiogenesis, 2024. 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 13 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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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.
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Who cites it
13 citing papers in PubMed, 15 citations in OpenAlex.
- Associations of Host Genetics and Plasma Proteomics with Incident Age-Related Macular Degeneration in Persons with AIDS.Ophthalmology science · 2026Article
- Emerging roles of granzymes in neurodegeneration and neuroinflammation: mechanistic insights and therapeutic opportunities.Acta neuropathologica · 2026Review
- FURIN Stimulates NOTCH2 and NOTCH3 Pathways, Leading to Return of Function in Aged Cells.Life (Basel, Switzerland) · 2026Article
- Identification and validation of platelet activation-related signatures in ulcerative colitis: a study based on machine learning and single-cell transcriptomic analysis.Frontiers in immunology · 2026Article
- Article
- Granzyme B from mast cells contributes to choroidal neovascularization in a model of wet age-related macular degeneration.Frontiers in immunology · 2026Article
- Granzyme B contributes to subretinal fibrosis in neovascular age-related macular degeneration by modulating inflammation and epithelial-mesenchymal transition.Journal of neuroinflammation · 2025Article
- Astrocytic RIPK3 exerts protective anti-inflammatory activity in mice with viral encephalitis by transcriptional induction of serpins.Science signaling · 2025Article
- Novel Circulating Biomarkers in Aortic Valve Stenosis.International journal of molecular sciences · 2025Review
- The pro-tumorigenic roles of granzyme B: mechanisms and therapeutic implications.Frontiers in immunology · 2025Review
- Changes in immune cell signatures during early infection reflect decoupling of capillary perfusion and glycocalyx dimensions.Frontiers in immunology · 2025Observational
- Mast cells promote choroidal neovascularization in a model of age-related macular degeneration.Journal of neuroinflammation · 2024Article
- Exploring the role of granzyme B in subretinal fibrosis of age-related macular degeneration.Frontiers in immunology · 2024Review
Corrections and comments
- Erratum issued
Authors and funding
20 authors at 3 institutions in 2 countries.
Funding
Abstract
Age-related macular degeneration (AMD) is a common retinal neurodegenerative disease among the elderly. Neovascular AMD (nAMD), a leading cause of AMD-related blindness, involves choroidal neovascularization (CNV), which can be suppressed by anti-angiogenic treatments. However, current CNV treatments do not work in all nAMD patients. Here we investigate a novel target for AMD. Granzyme B (GzmB) is a serine protease that promotes aging, chronic inflammation and vascular permeability through the degradation of the extracellular matrix (ECM) and tight junctions. Extracellular GzmB is increased in retina pigment epithelium (RPE) and mast cells in the choroid of the healthy aging outer retina. It is further increased in donor eyes exhibiting features of nAMD and CNV. Here, we show in RPE-choroidal explant cultures that exogenous GzmB degrades the RPE-choroid ECM, promotes retinal/choroidal inflammation and angiogenesis while diminishing anti-angiogenic factor, thrombospondin-1 (TSP-1). The pharmacological inhibition of either GzmB or mast-cell degranulation significantly reduces choroidal angiogenesis. In line with our in vitro data, GzmB-deficiency reduces the extent of laser-induced CNV lesions and the age-related deterioration of electroretinogram (ERG) responses in mice. These findings suggest that targeting GzmB, a serine protease with no known endogenous inhibitors, may be a potential novel therapeutic approach to suppress CNV in nAMD.
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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 Socratic graph.