ArticleBrain and behavior2025
KEAP1-NRF2/HO-1 Pathway Promotes Ferroptosis and Neuronal Injury in Schizophrenia.
Article in Brain and behavior, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Neuroimmune interactions: from molecular mechanisms to therapeutic targets.Molecular biomedicine · 2026Review
- Ferroptosis in Neuropsychiatric and Neurodegenerative Disorders: Shared Mechanisms and Disease-Specific Signatures.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Phytomedicines in preclinical and clinical research on antipsychotics-induced EPS/EPS-like behaviors: therapeutic effects and neurobiological mechanisms.Frontiers in psychiatry · 2026Review
- Nonpolysaccharide fraction ofFrontiers in pharmacology · 2026Article
- Coffee intake is associated with telomere length in severe mental disorders.BMJ mental health · 2025Article
Corrections and comments
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Authors and funding
3 authors.
Funding
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Abstract
backgroundThis study investigates the role of the KEAP1-NRF2/HO-1 signaling pathway in inducing ferroptosis and contributing to neuronal damage in schizophrenia.
methodsWe retrieved schizophrenia-related data and ferroptosis-related genes from the RNA microarray dataset GSE27383 and FerrDB database, respectively. Bioinformatics data identified KEAP1 as a downregulated gene, which was validated using qRT-PCR and Western blot. We assessed intracellular Fe
resultsPatients with schizophrenia exhibited underexpression of KEAP1, a key regulator of ferroptosis, along with elevated intracellular Fe
conclusionOur findings indicate that the KEAP1-NRF2/HO-1 pathway contributes to ferroptosis and neuronal injury in schizophrenia.
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