Evidence map›Paper›PMID 40324316›Full record

ReviewRedox biology2025

Oxidative stress response and NRF2 signaling pathway in autism spectrum disorder.

Sergio Davinelli, Alessandro Medoro, Martina Siracusano, Rosa Savino, Luciano Saso, Giovanni Scapagnini, Luigi Mazzone

Abstract readReview
In one paragraph

Review in Redox biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing 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

28 citing papers in PubMed.

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  12. Cell death-associated genes as novel diagnostic biomarkers for autism spectrum disorder.Apoptosis : an international journal on programmed cell death · 2026
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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

7 authors.

Sergio DavinelliDepartment of Medicine and Health Sciences "V. Tiberio", University of Molise, Campobasso, Italy.
Alessandro MedoroDepartment of Medicine and Health Sciences "V. Tiberio", University of Molise, Campobasso, Italy.
Martina SiracusanoDepartment of Biomedicine and Prevention, University of Rome Tor Vergata, Rome, Italy.
Rosa SavinoDepartment of Clinical and Experimental Medicine, University of Foggia, Foggia, Italy.
Luciano SasoDepartment of Physiology and Pharmacology "Vittorio Erspamer", Sapienza University of Rome, Rome, Italy.
Giovanni ScapagniniDepartment of Medicine and Health Sciences "V. Tiberio", University of Molise, Campobasso, Italy. Electronic address: giovanni.scapagnini@unimol.it.
Luigi MazzoneDepartment of Biomedicine and Prevention, University of Rome Tor Vergata, Rome, Italy; Child Neurology and Psychiatry Unit, Department of Wellbeing of Mental and Neurological, Dental and Sensory Organ Health, Policlinico Tor Vergata Hospital, Rome, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The prevalence of autism spectrum disorder (ASD), a neurodevelopmental disorder characterized by impairments in social communication and restricted/repetitive behavioral patterns, has increased significantly over the past few decades. The etiology of ASD involves a highly complex interplay of genetic, neurobiological, and environmental factors, contributing to significant heterogeneity in its clinical phenotype. In the evolving landscape of ASD research, increasing evidence suggests that oxidative stress, resulting from both intrinsic and extrinsic factors, may be a crucial pathophysiological driver in ASD, influencing neurodevelopmental processes that underlie behavioral abnormalities. Elevated levels of oxidative stress biomarkers, including lipid peroxides, protein oxidation products, and DNA damage markers, alongside deficient antioxidant enzyme activity, have been consistently linked to ASD. This may be attributed to dysregulated activity of nuclear factor erythroid 2-related factor 2 (NRF2), a pivotal transcription factor that maintains cellular redox homeostasis by orchestrating the expression of genes involved in antioxidant defenses. Here, we summarize the converging evidence that redox imbalance in ASD may result from NRF2 dysregulation, leading to reduced expression of its target genes. We also highlight the most promising antioxidant compounds under investigation, which may restore NRF2 activity and ameliorate ASD behavioral symptoms.

Indexed as

Autism Spectrum DisorderNF-E2-Related Factor 2Oxidative StressSignal TransductionAnimalsAntioxidantsBiomarkersHumansOxidation-ReductionAntioxidantsBiomarkersNFE2L2 protein, humanNF-E2-Related Factor 2AntioxidantsAutismInflammationNRF2Oxidative stress

Identifiers

PMID40324316
PMCPMC12099462

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.