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Updated: Jun 17, 2026
Oxygen-Induced Retinopathy Model for Ischemic Retinal Diseases in Rodents
Published on: September 16, 2020
Reactive Oxygen Species Regulation Across Retinitis Pigmentosa Animal Models: A 25-Year Systematized Review
Rafael de Freitas Azevedo-Repossi1,2, Rafael Brito3, Marcelo Cossenza4
1Laboratory of Gene Therapy and Viral Vector, Biophysics Graduate Program, Carlos Chagas Filho Institute of Biophysics, Universidade Federal Do Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil.
Abstract:
Retinitis pigmentosa (RP) is a progressive, inherited retinal disorder characterized by the degeneration of photoreceptor cells, leading to vision loss. Due to the heterogeneous nature of the mutations underlying RP, treatment options remain limited. Consequently, identifying common pathways involved in photoreceptor degeneration has become a priority in RP research. Several mechanisms, including activation of cell death pathways, inflammatory responses, and oxidative stress, have been consistently implicated across different mutations. The goal of this review was to analyze and identify, through a systematized search, data concerning reactive oxygen species (ROS) across animal models of the disease to comprehensively aggregate and discuss findings in each model over the last 25 years. In doing so, we highlight both shared mechanisms and model-specific differences, as well as identify gaps in the current literature. Our analysis reveals commonalities, such as the pivotal role of mitochondrial dysfunction in many models, alongside unique characteristics, such as variation in antioxidant responses depending on the specific genetic mutation. These insights can contribute to future research directions and help uncover new therapeutic targets within the context of oxidative stress in RP.
Insights
Reactive oxygen species (ROS) play a key role in inherited retinal diseases like retinitis pigmentosa (RP). This review analyzes ROS in RP animal models, revealing common pathways like mitochondrial dysfunction and model-specific antioxidant responses.
Area of Science:
- Ophthalmology
- Genetics
- Cell Biology
Background:
- Retinitis pigmentosa (RP) is an inherited retinal disorder causing progressive photoreceptor degeneration and vision loss.
- Limited treatment options for RP are due to the diverse genetic mutations involved.
- Identifying common mechanisms in photoreceptor degeneration is crucial for RP research.
Purpose of the Study:
- To systematically review and analyze data on reactive oxygen species (ROS) in animal models of retinitis pigmentosa over the past 25 years.
- To aggregate and discuss findings related to ROS across various RP models.
- To identify shared mechanisms and model-specific differences in ROS involvement and highlight research gaps.
Main Methods:
- Systematic literature search for studies on ROS in RP animal models.
- Analysis of data from the last 25 years.
- Aggregation and discussion of findings, comparing commonalities and differences across models.
Main Results:
- Consistent involvement of oxidative stress and ROS in photoreceptor degeneration across different RP models.
- Pivotal role of mitochondrial dysfunction identified as a common mechanism.
- Variations in antioxidant responses were observed, depending on the specific genetic mutation.
Conclusions:
- Oxidative stress and ROS are central to RP pathogenesis, with mitochondrial dysfunction being a key shared pathway.
- Understanding model-specific differences in ROS and antioxidant responses is essential.
- These insights can guide future research towards novel therapeutic targets for RP, focusing on oxidative stress pathways.
