Evidence map›Paper›PMID 41484209›Full record

ArticleScientific reports2026

Comprehensive transcriptomic analysis reveals canonical and novel pathways modulated by nanoceria in mammalian retinal degeneration.

L Donato, D Zerti, I Babiloni-Chust, M Passacantando, V Flati, M Feligioni, M Carl, C Rinaldi, L Poggi, R D'Angelo and 1 more

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In one paragraph

Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
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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

11 authors.

L Donato *Department of Biomedical and Dental Sciences and Morphofunctional Imaging, University of Messina, Messina, 98125, Italy.
D Zerti *Department of Biotechnological and Applied Clinical Sciences, University of L'Aquila, 67100, L'Aquila, Italy.
I Babiloni-ChustDepartment of Cellular, Computational and Integrative Biology (CIBIO), University of Trento, 38123, Trento, Italy.
M PassacantandoDepartment of Physical and Chemical Sciences, University of L'Aquila, 67100, L'Aquila, Italy.
V FlatiDepartment of Biotechnological and Applied Clinical Sciences, University of L'Aquila, 67100, L'Aquila, Italy.
M FeligioniFondazione European Brain Research Institute (EBRI) Rita Levi-Montalcini, Rome, Italy.
M CarlDepartment of Cellular, Computational and Integrative Biology (CIBIO), University of Trento, 38123, Trento, Italy.
C RinaldiDepartment of Biomedical and Dental Sciences and Morphofunctional Imaging, University of Messina, Messina, 98125, Italy.
L PoggiDepartment of Cellular, Computational and Integrative Biology (CIBIO), University of Trento, 38123, Trento, Italy.
R D'AngeloDepartment of Biomedical and Dental Sciences and Morphofunctional Imaging, University of Messina, Messina, 98125, Italy. rdangelo@unime.it.
R MaccaroneDepartment of Biotechnological and Applied Clinical Sciences, University of L'Aquila, 67100, L'Aquila, Italy.

Funding

Ministry of University and Research (MUR, Italy) through the PRIN (Progetti di Rilevante Interesse Nazionale) 2022 grant 2022PWMW5A
6 · The paper itself

Abstract

Retinal neurodegenerative diseases such as Age-related Macular Degeneration (AMD) and Retinitis Pigmentosa cause irreversible vision loss due to the limited regenerative capacity of the mammalian retina. Cerium oxide nanoparticles (nanoceria) are emerging therapeutics against oxidative stress and inflammation, major drivers of photoreceptor degeneration, and have demonstrated morphological and functional neuroprotection in preclinical models. However, the genome-wide transcriptional mechanisms underlying these effects remain incompletely characterized. We performed retinal transcriptomic analysis in a rat AMD model induced by intense light and treated intravitreally with nanoceria. Six groups were analyzed: control, light damage, vehicle, nanoceria, vehicle + light damage, and nanoceria + light damage. Light damage activated inflammatory and apoptotic programs, with upregulation of cytokines (Tnf, Il6, Il1b, Ccl2) and downregulation of photoreceptor genes (Rho, Pde6a/b, Gnat1). Nanoceria treatment counteracted these effects, suppressing pro-inflammatory mediators, restoring antioxidative genes (Nfe2l2, Gclc, Sod2), and enhancing neuroprotective factors (Bdnf, Cntf, Ngf). Pathway analyses revealed inhibition of TNF/NF-κB/IL-17 signaling and activation of PI3K-Akt, JAK-STAT, and neurotrophin pathways. Unexpectedly, nanoceria also modulated amino acid and insulin metabolism (Ass1, Cps1, Insr, Irs1, Slc2a4) and reactivated transcription factors (Ascl1, Sox2, Notch1) typically silent in adult retina. Our findings highlight nanoceria as a multifunctional therapeutic that mitigates retinal degeneration by coordinating oxidative, inflammatory, and regenerative responses. Together with prior morphological and functional validations, these results support the translational potential of nanoceria for treating retinal neurodegenerative diseases.

Indexed as

CeriumRetinal DegenerationTranscriptomeAnimalsDisease Models, AnimalGene Expression ProfilingLightMaleNanoparticlesOxidative StressRatsRetinaSignal Transductionceric oxideCeriumNanoceriaNeuroinflammatory modulationOxidative stress modulationRegenerative responsesRetinal degenerationTranscriptomic analysis

Identifiers

PMID41484209
PMCPMC12852738

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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.