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Updated: Mar 21, 2026
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Author Spotlight: Establishing a Practical and Cost-Effective Protocol for Corneal Sensitivity Testing in Clinical Settings
Published on: August 2, 2024
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[To Protect Corneal Transparency against Diseases]
Nippon Ganka Gakkai Zasshi
|May 12, 2016
Summary
New nucleic acid drugs show promise for treating corneal neovascularization, scarring, and TGFBI-related dystrophy. Topical RNAi targeting Angptl2 inhibits neovascularization, while Angptl7 modulation and CRISPR gene editing offer novel therapeutic avenues for corneal diseases.
Area of Science:
- Ophthalmology
- Molecular Biology
- Gene Therapy
Context:
- Corneal neovascularization, scarring, and TGFBI-related corneal dystrophy threaten vision.
- Current treatments are limited, necessitating novel therapeutic strategies.
- Nucleic acid drugs offer a promising approach for ocular surface diseases.
Purpose:
- To develop novel nucleic acid-based therapies for corneal neovascularization, corneal scar, and TGFBI-related corneal dystrophy.
- To investigate the role of angiopoietin-like proteins (Angptl2 and Angptl7) in corneal diseases.
- To explore CRISPR-Cas9 gene editing for treating genetic corneal disorders.
Summary:
- Topical application of a modified RNA interference (RNAi) molecule targeting angiopoietin-like protein 2 (Angptl2) inhibited corneal neovascularization and scarring in a mouse model.
- Angiopoietin-like protein 7 (Angptl7) was identified as a molecule with dual anti-angiogenic and neurotrophic properties in the cornea, suggesting its potential therapeutic use.
- CRISPR-Cas9 mediated homology directed repair (HDR) successfully corrected the genetic defect in R124H granular dystrophy in patient-derived corneal keratocytes in vitro.
Impact:
- This research introduces a novel topical RNAi formulation for corneal neovascularization and scar treatment.
- Modulating Angptl7 presents a new therapeutic strategy for protecting corneal transparency through its unique biological functions.
- CRISPR-Cas9 gene editing holds potential as a future radical treatment for inherited TGFBI-related corneal dystrophies.
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