ArticleMethods in molecular biology (Clifton, N.J.)2017
Demonstrating Potential of Cell Therapy for Wilson's Disease with the Long-Evans Cinnamon Rat Model.
Article in Methods in molecular biology (Clifton, N.J.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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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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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
8 citing papers in PubMed.
- A Multi-Gene Signature Associated with 1-Year Survival in Patients with Stage I Liver Cancer: Integration of Preclinical and TCGA Data.Current issues in molecular biology · 2026Article
- Neuro-regeneration or Repair: Cell Therapy of Neurological Disorders as A Way Forward.Current neuropharmacology · 2024Review
- CationicMolecules (Basel, Switzerland) · 2022Article
- Efficient Reconstitution of Hepatic Microvasculature by Endothelin Receptor Antagonism in Liver Sinusoidal Endothelial Cells.Human gene therapy · 2019Article
- Therapeutic potential of hepatocyte-like-cells converted from stem cells from human exfoliated deciduous teeth in fulminant Wilson's disease.Scientific reports · 2019Article
- InGene expression · 2018Article
- DPM-1001 decreased copper levels and ameliorated deficits in a mouse model of Wilson's disease.Genes & development · 2018Article
- Wilson's disease: Prospective developments towards new therapies.World journal of gastroenterology · 2017Review
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Wilson's disease (WD) is characterized by the inability to excrete copper (Cu) from the body with progressive tissue injury, especially in liver and brain. The molecular defect in WD concerns mutations in ATP7B gene leading to loss of Cu transport from the hepatocyte to the bile canaliculus. While drugs, e.g., Cu chelators, have been available for several decades, these must be taken lifelong, which can be difficult due to issues of compliance or side effects. Many individuals may require liver transplantation, which can also be difficult due to donor organ shortages. Therefore, achieving permanent cures via cell or gene therapy are of great interest for WD. Cell therapy is feasible because transplanted hepatocytes can integrate in liver parenchyma and restore deficient functions, including transport of Cu into bile. The availability of authentic animal models that recapitulate hepatic WD, especially the Long-Evans Cinnamon (LEC) rat, has advanced cell transplantation research in WD. We describe requirements for cell therapy in animal models with several standardized methods for studies to test or refine cell therapy strategies in WD.
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