Corneal neovascularization: updates on pathophysiology, investigations &amp; management

Sharif, Zainab; Sharif, Walid

doi:10.22336/rjo.2019.4

Cited by 133 publications

(103 citation statements)

References 42 publications

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“…Corneal neovascularization (CNV) involves the ingrowth of new blood vessels from the limbus into the avascular cornea [1-3]. These new vessels disrupt corneal clarity, which threatens vision [3].…”

Section: Introductionmentioning

confidence: 99%

Resolution of Refractory Corneal Neovascularization with Subconjunctival Bevacizumab

Britton¹,

Crayford²

2020

Case Rep Ophthalmol

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Corneal neovascularization (CNV) has a variety of causes and threatens corneal clarity, thus optimal visual acuity. Conventional medical management includes topical steroids and matrix metalloproteinase inhibitors like doxycycline. Anti-vascular endothelial growth factor (anti-VEGF) agents have demonstrated promise but remain off-label for this indication. However, these agents hold value in cases refractory to first-line medical management. We report the case of a 63-year-old woman who presented with ocular rosacea and CNV affecting vision, on a background of acne rosacea. She was initially treated with fluorometholone and doxycycline, yet continued to deteriorate. Eventually she received two 1.5-mg subconjunctival injections of bevacizumab 2 months apart. CNV completely resolved and results were maintained at 4-year follow-up. This case demonstrates that refractory CNV can be effectively treated with subconjunctival injection of anti-VEGF bevacizumab. The resolution of CNV was also maintained years after injection with minimal adjunctive therapy during this period, and to our knowledge there are no other studies reporting a follow-up period of 4 years after treatment. This is a pertinent case for other clinicians treating patients in a similar situation.

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Section: Introductionmentioning

confidence: 99%

Resolution of Refractory Corneal Neovascularization with Subconjunctival Bevacizumab

Britton¹,

Crayford²

2020

Case Rep Ophthalmol

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“…Corneal transparency partly depends on the balance between angiogenesis and anti-angiogenesis related essentials. The corneal stroma could be intruded by abnormal neovessels once the balance fails, which usually induces the damages of normal structures and the neovascularization [2]. Corneal neovascularization may arise from various reasons, comprising degenerative, infectious and in ammatory factors, etc., leading to the pathological angiogenesis [3,4].…”

Section: Introductionmentioning

confidence: 99%

GDF15 Promotes Corneal Neovascularization and Retinoblastoma Cell Progression via AKT/ERK Signal Pathway

Wen¹,

Cheng²,

Li³

et al. 2020

Preprint

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Objective: We performed this study to investigate the role of growth differentiation factor 15 (GDF15) in corneal neovascularization and retinoblastoma cell progression and the potential mechanisms.Methods: Human retinal endothelial cell (HREC) and retinoblastoma cell line (Y79, RB116 and WERI-Rb1) were treated with recombinant human (rhGDF15, 50 ng/mL) and transfected with small interfering RNA, si-GDF15. Cell migration and proliferation were detected by Scratch assay and CCK8 assay. We performed flow cytometry to measure apoptosis. Tube formation assay for in vitro angiogenesis measurement was used. RT-PCR and western blot were applied to detect the angiogenesis-related factors expression and the level of p-AKT(Ser473), p-AKT(Thr308), AKT, p-ERK1/2(Thr202/Tyr204), and ERK1/2. Tumor growth curve was used after subcutaneous injection of Y79 cells in nude mice and rhsi-GDF15 injection into the tail vein during 21 days.Results: In retinoblastoma cell, rhGDF15 promoted Y79, RB116 and WERI-Rb1 cell migration and suppressed the level of apoptosis. The knock-down of GDF15 significantly inhibited cell migration and promoted apoptosis. In HREC, rhGDF15 increased the tube formation, the level of HIF-1α and SDF, and cell migration, compared with control group, and si-GDF15 played the opposite role. The level of p-AKT(Ser473), p-AKT(Thr308), AKT, p-ERK1/2(Thr202/Tyr204), and ERK1/2 were increased by rhGDF15 in both HREC and retinoblastoma cell lines, contrary to the results of GDF15 knock-down.Conclusion: The downregulation of GDF15 can inhibit corneal angiogenesis and the migration of retinoblastoma cells and promote their apoptosis, which could be dependent on the AKT/ERK pathway.

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“…Corneal neovascularization (CNV) is ingrowth of new vessels from the limbus, which can cause visual loss due to accompanying scarring and lipid deposition [1,2]. It results from acute or chronic corneal inflammation, limbal stem cell deficiency, and corneal ischemia [1,2]. Corneal angiogenesis is initiated by the imbalance between angiogenic and anti-angiogenic factors [2,3].…”

Section: Introductionmentioning

confidence: 99%

“…It results from acute or chronic corneal inflammation, limbal stem cell deficiency, and corneal ischemia [1,2]. Corneal angiogenesis is initiated by the imbalance between angiogenic and anti-angiogenic factors [2,3]. Angiogenic factors, including vascular endothelial growth factor (VEGF), hypoxia-inducible factor (HIF), matrix metalloproteinases (MMPs), platelet-derived growth factor (PDGF), and basic fibroblast growth factor (FGF) are upregulated during corneal angiogenesis, whereas the anti-angiogenic factors are downregulated [2,3].…”

Section: Introductionmentioning

confidence: 99%

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Comparison of the Therapeutic Efficacies of Topical Rivoceranib and Topical Bevacizumab in a Murine Model of Corneal Neovascularization

Yoon

Woo

et al. 2019

Medicina

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Background and Objectives: Corneal neovasculariziation (CNV) is a serious vision-threatening complication; however, all therapeutics have their clinical limitations. The aim of this study is to investigate the efficacy of topical rivoceranib compared with topical bevacizumab in a murine model of corneal neovascularization (CNV). Materials and Methods: Murine CNV was induced by means of total de-epithelization and alkali burn. Mice were divided into five groups according to topical treatment: untreated control, phosphate-buffered saline (PBS), 0.1% and 0.5% rivoceranib, and 0.5% bevacizumab. CNV area and index were measured 7 and 14 days after treatment. After corneal tissues were excised at day 14, the blood and lymphatic vessels were quantified by cluster of differentiation 31 (CD31) and lymphatic vessel endothelial hyaluronan receptor 1 (LYVE1) immunofluorescence, respectively. Results: After 14 days, treatment groups with 0.1% and 0.5% rivoceranib and 0.5% bevacizumab showed a decrease in CNV area and index compared with the untreated and PBS groups (all p < 0.01). Blood and lymphatic vascularization significantly decreased in the 0.5% rivoceranib and 0.5% bevacizumab groups, as measured by CD31 and LYVE1 immunofluorescence. There was no significant difference of vascularization between the 0.5% rivoceranib and bevacizumab groups. Conclusions: Topical application of rivoceranib could effectively decrease CNV equivalent to topical bevacizumab in a murine model.

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Corneal neovascularization: updates on pathophysiology, investigations & management

Cited by 133 publications

References 42 publications

Resolution of Refractory Corneal Neovascularization with Subconjunctival Bevacizumab

Resolution of Refractory Corneal Neovascularization with Subconjunctival Bevacizumab

GDF15 Promotes Corneal Neovascularization and Retinoblastoma Cell Progression via AKT/ERK Signal Pathway

Comparison of the Therapeutic Efficacies of Topical Rivoceranib and Topical Bevacizumab in a Murine Model of Corneal Neovascularization

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