ArticleRedox biology2026
Repurposing melatonin's therapeutic potential in Wilson disease: Addressing copper overload and redox imbalance.
Article in Redox biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
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Who cites it
3 citing papers in PubMed.
- Subtype-Specific Alterations in Copper Trafficking Associated with KRAS Mutations in Isogenic Colorectal Cancer Cell Lines.Biological trace element research · 2026Article
- Sequence-Defined Short Peptide-Derived Coacervate Vesicles for Targeted Therapeutics.Advanced materials (Deerfield Beach, Fla.) · 2026Article
- Physiological and Proteomic Insights into Melatonin-Mediated Regulation of Copper Toxicity in the CrayfishInternational journal of molecular sciences · 2026Article
Corrections and comments
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Authors and funding
18 authors.
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Abstract
Loss-of-function mutations in copper-ATPase ATP7B underlie Wilson disease (WD), a disorder characterized by hepatic copper accumulation and severe hepato-neuropathology. Existing chelation therapeutics remove excess copper but lack intrinsic antioxidant capacity and frequently cause systemic toxicity. Here we evaluate melatonin, an FDA-approved indoleamine with antioxidant and putative metal-chelating activity, as a candidate therapeutic for WD. In ATP7B
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Registered trials
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