A method for establishing a concurrent cataract mouse model

By knocking out the Phb2 gene in the mouse retina using CRISPR/Cas9 gene editing technology, the Phb2flox/flox;Six3-Cre mouse model was constructed, which solved the problems of insufficient etiological simulation and reproducibility of existing models, and realized the effective simulation of concurrent cataracts and the exploration of treatment strategies.

CN120304360BActive Publication Date: 2026-07-03ZHONGSHAN OPHTHALMIC CENT SUN YAT SEN UNIV
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Patent Information

Authority / Receiving Office
CN · China
Patent Type
Patents(China)
Current Assignee / Owner
ZHONGSHAN OPHTHALMIC CENT SUN YAT SEN UNIV
Filing Date
2025-04-21
Publication Date
2026-07-03

AI Technical Summary

Technical Problem

Existing animal models of concurrent cataracts are insufficient in terms of etiological simulation, reproducibility, and clinical relevance. They are difficult to effectively simulate chronic inflammatory processes such as uveitis or cataracts related to metabolic diseases. Furthermore, the procedures are complex and the success rate is greatly affected by the surgeon's experience.

Method used

Phb2flox/flox;Six3-Cre mouse models were constructed by knocking out the Phb2 gene in the mouse retina using CRISPR/Cas9 gene editing technology, which simulated the pathogenesis and pathological characteristics of human complicated cataracts.

Benefits of technology

This study provides an experimental model that is similar to the clinical phenotype of complicated cataracts, which can be used to study the pathogenesis of complicated cataracts and explore treatment strategies, providing theoretical basis and experimental support for clinical treatment.

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Abstract

The application discloses a method for establishing a concurrent cataract mouse model, and the mouse model is obtained by retinal-specific knockout of a Phb2 gene. flox / flox The Six3-Cre mouse appears a degenerative retinal disease phenotype at the age of 6-8 weeks, fundus examination shows that the retina is atrophic and thin, the structure of each layer is disordered, the distribution of retinal pigment is disordered, and electrophysiological examination shows that the mouse has abnormal vision function. The mouse appears lens opacity at the age of 8-10 months, and shows a concurrent cataract phenotype. Therefore, the model mouse can better simulate the phenotype of concurrent cataract in clinic, and can be used as an animal model for concurrent cataract related research.
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