ArticleInternational journal of molecular sciences2025
Evidence of Oxytosis/Ferroptosis in Niemann-Pick Disease Type C.
Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
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Who cites it
5 citing papers in PubMed.
- Ferroptosis-related stress during aging and its relevance to disease.GeroScience · 2026Review
- Omega-3 Fatty Acids Attenuate Neuropathic Pain by Modulating Ferroptotic Stress, Selenoamino Acid Metabolism, and Lipid Remodeling.Antioxidants (Basel, Switzerland) · 2026Article
- Sustained dysregulation of iron and glutathione homeostasis induces chronoferroptosis, a persistent ferroptotic adaptation in neuronal cells.Cell death discovery · 2026Article
- Neurodegenerative Disease: From Molecular Basis to Therapy, 3rd Edition.International journal of molecular sciences · 2026Article
- From autophagy-lysosomal deficits to neurodegeneration in Niemann-Pick type C1 disease: implications for age-related neurodegenerative disorders.Frontiers in neuroscience · 2026Review
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Authors and funding
12 authors.
Funding
Abstract
Niemann-Pick Disease Type C (NPC) is a hereditary neurodegenerative disease characterized by selective cell vulnerability, particularly affecting cerebellar anterior Purkinje neurons. These neurons exhibit a distinctive pattern of degeneration due to the loss of NPC1 and/or NPC2 protein function, progressively extending towards posterior cerebellar regions. Our study aimed to explore the early factors influencing this selective vulnerability of anterior Purkinje neurons in NPC. Oxytosis/ferroptosis, a novel form of regulated cell death, has been implicated in neurodegenerative diseases, with its inhibition showing promising therapeutic potential. Our laboratory has previously identified parallels between NPC cellular pathology and ferroptotic markers, including elevated levels of lipid peroxidation and iron, mitochondrial dysfunction, and Ca
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