ArticleProceedings of the National Academy of Sciences of the United States of America2023
FDX1-dependent and independent mechanisms of elesclomol-mediated intracellular copper delivery.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
97 citing papers in PubMed, 1 synthesis or guideline pooled it, 120 citations in OpenAlex.
- Cuproptosis: Mechanisms, biological significance, and advances in disease treatment-A systematic review.CNS neuroscience & therapeutics · 2024Pooled it
- The role of copper and cuproptosis in digestive system cancers: novel therapeutic strategies and mechanistic insights.Cancer biology & therapy · 2026Review
- Cuproptosis and the bioinorganic basis of copper-induced cell death.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2026Review
- GSH-responsive self-assembled nanoplatform synergistically enhances cuproptosis through metabolic reprogramming and oxidative stress amplification.Materials today. Bio · 2026Article
- Effects of copper overload on mitochondrial parameters in GBM-1, U-87 MG, and C6 glioma cell lines.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026Article
- FDX1-short proteoform induces caspase-independent cell death in tumor cells.Cell death and differentiation · 2026Article
- Cuproptosis and ferroptosis: signal pathways, diseases and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Cuproptosis in Ischemic Stroke: Molecular Mechanisms and Therapeutic Potential.Molecules (Basel, Switzerland) · 2026Review
- Cuproptosis in iron overload hepatocytes.Cell death & disease · 2026Article
- Cunermuspir, a Copper(I)-Niacin Complex, Modulates Mitochondrial Respiration and Cellular Oxidant Handling in Fibroblasts from Children with Autism Spectrum Disorder.Antioxidants (Basel, Switzerland) · 2026Article
- SIRT5 mediates the pro-osteogenic effects of estrogen through FDX1 demalonylation and cuproptosis inhibition in mesenchymal stem cells.Genes & diseases · 2026Article
- Review
- The Role of Metal Ions in Mitochondria: From Energy Metabolism to Cell Destiny.Biological trace element research · 2026Review
- Targeting Copper in Cancer: Chelators to Counteract Cuproplasia and Ionophores to Promote Cuproptosis.Journal of medicinal chemistry · 2026Review
- Copper homeostasis and cuproptosis rewire the tumor microenvironment: mechanisms, immune modulation, and therapeutic opportunities.Journal of hematology & oncology · 2026Review
- Beyond apoptosis: nanomedicine enabled reprogramming of tumor cell death for next-generation radiosensitization.Journal of nanobiotechnology · 2026Review
- Copper homeostasis and cuproptosis: molecular mechanisms and therapeutic opportunities.Molecular biomedicine · 2026Review
- Cuproptosis Inducers in Cancer Therapy: State of the Art and Challenges.Chemical record (New York, N.Y.) · 2026Review
- Role of Ferredoxin 1Cancer pathogenesis and therapy · 2026Review
- SLC25A3 exports mitochondrial copper to metalate cytochromeProceedings of the National Academy of Sciences of the United States of America · 2026Article
37 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
13 authors at 5 institutions in 1 country.
Funding
Abstract
Recent studies have uncovered the therapeutic potential of elesclomol (ES), a copper-ionophore, for copper deficiency disorders. However, we currently do not understand the mechanism by which copper brought into cells as ES-Cu(II) is released and delivered to cuproenzymes present in different subcellular compartments. Here, we have utilized a combination of genetic, biochemical, and cell-biological approaches to demonstrate that intracellular release of copper from ES occurs inside and outside of mitochondria. The mitochondrial matrix reductase, FDX1, catalyzes the reduction of ES-Cu(II) to Cu(I), releasing it into mitochondria where it is bioavailable for the metalation of mitochondrial cuproenzyme- cytochrome
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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.