ArticleBMC biology2025
Transcriptomic signatures of oxytosis/ferroptosis are enriched in Alzheimer's disease.
Article in BMC biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Multi-omics technologies: Novel tools and methods for assessing nerve injury and regeneration.Neural regeneration research · 2026Article
- Ferroptosis-related stress during aging and its relevance to disease.GeroScience · 2026Review
- Ferroptosis and aging: Inducing and catalyzing neurodegenerative diseases.Neural regeneration research · 2026Article
- Targeting Ferroptosis Pathways for Synaptic Protection in Sevoflurane-Induced Cognitive Impairment: A Nanomedicine Approach.CNS neuroscience & therapeutics · 2026Review
- Non-canonical cell death in neurodegeneration: emerging mechanisms and therapeutic Frontiers.Apoptosis : an international journal on programmed cell death · 2026Review
- The dual role of ATF4 in neurons: from stress adaptation to therapeutic intervention.Frontiers in molecular neuroscience · 2026Review
- Traditional Chinese Medicine and Ferroptosis in Alzheimer's Disease: A Potential Therapeutic Approach.Drug design, development and therapy · 2026Review
- Metabolic cell death networks in Alzheimer's disease: mechanistic links and therapeutic perspectives of ferroptosis, cuproptosis, and disulfidptosis.Frontiers in cell and developmental biology · 2026Review
- Exercise mitigates Alzheimer's disease by targeting ferroptosis driven by cellular senescence.Frontiers in cell and developmental biology · 2025Review
- Ferroptosis in Alzheimer's disease: molecular mechanisms and advances in therapeutic strategies.Frontiers in neuroscience · 2025Review
- Neuroprotective and anti-inflammatory activity ofFrontiers in pharmacology · 2025Article
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7 authors.
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Abstract
backgroundOxytosis/ferroptosis is a form of non-apoptotic regulated cell death characterized by specific changes in the redox balance that lead to lethal lipid peroxidation. It has been hypothesized recently that aging predisposes the brain to the activation of oxytosis/ferroptosis in Alzheimer's disease (AD), and consequently that inhibition of oxytosis/ferroptosis offers a path to develop a new class of therapeutics for the disease. The goal of the present study was to investigate the occurrence of oxytosis/ferroptosis in the AD brain by examining transcriptomic signatures of oxytosis/ferroptosis in cellular and animal models of AD as well as in human AD brain samples.
resultsSince oxytosis/ferroptosis has been poorly defined at the RNA level, the publicly available datasets are limited. To address this limitation, we developed TrioSig, a gene signature generated from transcriptomic data of human microglia, astrocytes, and neurons treated with inducers of oxytosis/ferroptosis. It is shown that the different signatures of oxytosis/ferroptosis are enriched to varying extents in the brains of AD mice and human AD patients. The TrioSig signature was the most frequently found enriched, and bioinformatic analysis of its composition identified genes involved in the integrated stress response (ISR). It was confirmed in nerve cell culture that oxytosis/ferroptosis induces the ISR via phosphorylation of eukaryotic translation initiation factor 2 alpha (eIF2α) and activating transcription factor 4 (ATF4) signaling.
conclusionsOur data support the involvement of oxytosis/ferroptosis in AD. The implications of the ISR for the progression and prevention of AD are discussed.
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