Evidence map›Paper›PMID 40739380›Full record

ReviewMolecular neurobiology2025

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

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

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Review
  2. Article
  3. Icariin Against Neurodegeneration: A Focus in Cell Death Pathways.International journal of molecular sciences · 2026
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Rafael de Freitas Azevedo-RepossiLaboratory 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.
Rafael BritoLaboratory of Neuronal Physiology and Pathology, Department of Cellular and Molecular Biology, Institute of Biology, Neuroscience Graduate Program, Universidade Federal Fluminense, Niterói, Rio de Janeiro, Brazil.
Marcelo CossenzaLaboratory of Molecular Pharmacology, Department of Physiology and Pharmacology, Biomedical Institute, Graduate Program in Neurosciences, Biology Institute, Universidade Federal Fluminense, Niterói, Rio de Janeiro, Brazil.ORCID http://orcid.org/0000-0001-8636-964X
Alexandre Dos Santos-RodriguesNeurobiology of Cellular Interactions Laboratory, Department of Neurobiology, Institute of Biology, Neuroscience Graduate Program, Universidade Federal Fluminense, Niterói, Rio de Janeiro, Brazil.
Gustavo Costa FerreiraLaboratory of Inborn Errors of Metabolism, Institute of Medical Biochemistry Leopoldo de Meis, Universidade Federal Do Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil.
Hilda Petrs-SilvaLaboratory 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.
Karin C Calaza *Neurobiology of the Retina Laboratory, Department of Neurobiology, Institute of Biology, Neuroscience Graduate Program, Universidade Federal Fluminense, Niterói, Rio de Janeiro, Brazil.
Lucianne Fragel-Madeira *Neural Degeneration and Regeneration Laboratory, Department of Neurobiology, Institute of Biology, Neuroscience Graduate Program, Universidade Federal Fluminense, Niterói, Rio de Janeiro, Brazil. lfragel@id.uff.br.ORCID http://orcid.org/0000-0001-6747-2828

Funding

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior 001
6 · The paper itself

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.

Indexed as

Reactive Oxygen SpeciesRetinitis PigmentosaAnimalsDisease Models, AnimalHumansOxidative StressReactive Oxygen SpeciesHereditary RetinopathiesNeurodegenerationOxidative stressRetinaSystematized review

Identifiers

PMID40739380

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.