ArticleCell death & disease2020
Intracellular amyloid toxicity induces oxytosis/ferroptosis regulated cell death.
Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.
What it found
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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.
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Who cites it
78 citing papers in PubMed, 121 citations in OpenAlex.
- Discovery and preclinical validation of a translationally optimized mitochondrial complex I modulator for Alzheimer's disease.npj drug discovery · 2026Article
- Multi-omics technologies: Novel tools and methods for assessing nerve injury and regeneration.Neural regeneration research · 2026Article
- Prominin 2 promotes the progression of breast cancer by inhibiting ferroptosisJournal of translational internal medicine · 2026Article
- Ferroptosis-related stress during aging and its relevance to disease.GeroScience · 2026Review
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- Metabolic Reprogramming Associated with Ferroptosis Protection by an Indole-Based Antioxidant in Aβ(25-35)-Treated SH-SY5Y Cells.Antioxidants (Basel, Switzerland) · 2026Article
- A High-Throughput Assay for Monitoring and Quantifying Amyloid-β Accumulation and Clearance in Alzheimer's Disease Cell Models.Journal of neurochemistry · 2026Article
- Inhibition of EPAC1 Prevents Neuronal Death Mediated by Diesel Exhaust Particles in Ferroptotic Cell Death Conditions.Antioxidants (Basel, Switzerland) · 2026Article
- Discovery and Preclinical Validation of a Clinically Optimized Mitochondrial Complex I Modulator for Alzheimer's Disease.bioRxiv : the preprint server for biology · 2026Article
- RNA-binding activity of PHGDH drives amyloid-beta production in a human brain organoid model of sporadic Alzheimer's disease.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Novel Small-Molecule Analogues of IU1 Ameliorate Amyloid-β Mediated Toxicity in Alzheimer's Disease Cell and Worm Models.International journal of molecular sciences · 2026Article
- Multi-Omics Evidence Based on Spatial Transcriptomics Data Reveals the Therapeutic Value of Copper Death Genes in Glioblastoma.International journal of genomics · 2026Article
- Ferroptosis and Alzheimer's disease: unraveling the molecular mechanisms and therapeutic opportunities.Frontiers in cell and developmental biology · 2026Review
- Ferroptosis and Alzheimer's disease: a new insight into neurodegeneration.Frontiers in immunology · 2026Review
- A high-throughput, quantitative platform using 2D dissociated human cerebral organoids to model neuroinflammation in Alzheimer's disease.NPJ dementia · 2026Article
- Ferroptosis-associated RNA-binding proteins predict clinical outcomes in head and neck squamous cell carcinoma.Translational cancer research · 2025Article
- From mechanism to application: programmed cell death pathways in nanomedicine-driven cancer therapies.Bioactive materials · 2025Review
- Unveiling Moxibustion's Impact on AD Mice Learning and Memory: Role of Mitochondrial Respiratory Chain Complex I Subunit in the Hippocampus.Molecular neurobiology · 2025Article
- MiR-7a-Klf4 axis as a regulator and therapeutic target of neuroinflammation and ferroptosis in Alzheimer's disease.NAR molecular medicine · 2025Article
18 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Amyloid beta (Aβ) accumulates within neurons in the brains of early stage Alzheimer's disease (AD) patients. However, the mechanism underlying its toxicity remains unclear. Here, a triple omics approach was used to integrate transcriptomic, proteomic, and metabolomic data collected from a nerve cell model of the toxic intracellular aggregation of Aβ. It was found that intracellular Aβ induces profound changes in the omics landscape of nerve cells that are associated with a pro-inflammatory, metabolic reprogramming that predisposes cells to die via the oxytosis/ferroptosis regulated cell death pathway. Notably, the degenerative process included substantial alterations in glucose metabolism and mitochondrial bioenergetics. Our findings have implications for the understanding of the basic biology of proteotoxicity, aging, and AD as well as for the development of future therapeutic interventions designed to target the oxytosis/ferroptosis regulated cell death pathway in the AD brain.
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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.