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<p>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&#xa0;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.</p>

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Reactive Oxygen Species Regulation Across Retinitis Pigmentosa Animal Models: A 25-Year Systematized Review

  • 期刊论文

  • 发表日期：

    2025年7月30日

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  • Rafael de Freitas Azevedo-Repossi,
  • Rafael Brito,
  • Marcelo Cossenza,
  • Alexandre dos Santos-Rodrigues,
  • Gustavo Costa Ferreira,
  • Hilda Petrs-Silva,
  • Karin C. Calaza,
  • Lucianne Fragel-Madeira

摘要

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.