# Rodent Models of Glaucoma: How Mice and Rats Can Help Human Vision Move Out of the Woods and Into the Light

## TL;DR

This paper reviews rodent models of glaucoma to better understand and treat the disease, which is a growing health concern.

## Contribution

The paper systematically reviews rodent models of glaucoma, highlighting their strengths and limitations for translational research.

## Key findings

- Rodent models can replicate key aspects of glaucoma, including intraocular pressure elevation and retinal ganglion cell degeneration.
- Genetic models like DBA/2J and others provide insights into specific glaucoma-related genes and pathways.
- Combining different rodent models may help overcome the disease's heterogeneity and improve clinical translation.

## Abstract

Glaucoma represents a social and economic burden due to both its increasing incidence and the lack of knowledge about its physiopathology and treatment strategies. The main factor hindering progress in glaucoma research is the disease’s heterogeneity, which depends on both genetic and environmental factors. This limitation directly affects glaucoma research, posing obstacles to the elucidation of risk factors, disease mechanisms, and treatment strategies. Therefore, the need emerges to integrate pre-clinical experimental observations from different experimental models to recapitulate different aspects of the disease and achieve a successful translation to clinics. Here, we reviewed the glaucoma models that are currently available for basic and translational research, with a specific focus on models based on rodents. Regarding genetic glaucoma models, we considered the main hallmarks and limitations of DBA/2J, glutamate/aspartate transporter/excitatory amino acid carrier 1, myocilin, connective tissue growth factor, optineurin, purinergic receptor 2Y, caveolin 1, and endothelin-1 mice. Regarding other glaucoma models, we considered rodent models based on intraocular pressure elevation via perturbation of aqueous humor dynamics or on direct degeneration of retinal ganglion cells via physical or chemical damage.