ArticleNutrients2021
Retinal Neurodegeneration: Correlation between Nutraceutical Treatment and Animal Model.
Article in Nutrients, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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.
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.
Who cites it
12 citing papers in PubMed, 12 citations in OpenAlex.
- Targeting Neurodegeneration With Naringenin: Mechanistic Perspectives and Therapeutic Implications.Molecular nutrition & food research · 2026Review
- Photoreceptor preservation by FAAH inhibition in a murine model of retinitis pigmentosa.Molecular neurobiology · 2026Article
- Saffron as a Retinal Neuroprotectant: A Narrative Review of Preclinical Studies and Clinical Results.Antioxidants (Basel, Switzerland) · 2026Review
- A Window to the Brain: The Retina to Monitor the Progression and Efficacy of Saffron RepronPharmaceuticals (Basel, Switzerland) · 2023Article
- Autophagy in the retinal neurovascular unit: New perspectives into diabetic retinopathy.Journal of diabetes · 2023Review
- Resveratrol-like Compounds as SIRT1 Activators.International journal of molecular sciences · 2022Article
- Silencing of circular RNA‑ZYG11B exerts a neuroprotective effect against retinal neurodegeneration.International journal of molecular medicine · 2022Article
- Naringenin upregulates GTPCH1/eNOS to ameliorate high glucose-induced retinal endothelial cell injury.Experimental and therapeutic medicine · 2022Article
- Nutraceutical Molecules Slow Down Retinal Degeneration, in Tvrm4 Mice a Model of Retinitis Pigmentosa, by Genetic Modulation of Anti-oxidant Pathway.Frontiers in neuroscience · 2022Article
- Long-term oral administration of naringenin counteracts aging-related retinal degenerationFrontiers in pharmacology · 2022Article
- Review
- Sequential PBM-Saffron Treatment in an Animal Model of Retinal Degeneration.Medicina (Kaunas, Lithuania) · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Retinal diseases can be induced by a variety of factors, including gene mutations, environmental stresses and dysmetabolic processes. The result is a progressive deterioration of visual function, which sometimes leads to blindness. Many treatments are under investigation, though results are still mostly unsatisfactory and restricted to specific pathologies, particularly in the case of gene therapy. The majority of treatments have been tested in animal models, but very few have progressed to human clinical trials. A relevant approach is to study the relation between the type of treatments and the degenerative characteristics of the animal model to better understand the effectiveness of each therapy. Here we compare the results obtained from different animal models treated with natural compounds (saffron and naringenin) to anticipate the potentiality of a single treatment in different pathologies.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.