ReviewInternational journal of molecular sciences2015
Wilson's disease: a comprehensive review of the molecular mechanisms.
Review in International journal of molecular sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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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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
49 citing papers in PubMed, 116 citations in OpenAlex.
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- Glutathione Biology in Neurodegenerative and Metabolic Diseases: Molecular Mechanisms, Pathophysiological Roles, and Therapeutic Perspectives.International journal of molecular sciences · 2026Review
- Liver-nervous system axis: pathways, dysregulation, and translational perspectives.Journal of neuroinflammation · 2026Review
- Copper Homeostasis and Cuproptosis in Neurological Disorders.Drug design, development and therapy · 2026Review
- Diagnosis and Potential Therapy of Brain Diseases UsingCurrent medicinal chemistry · 2026Article
- Human CTR1 Through the Ages: Milestones and Emerging Roles in Disease and Therapy.Biomolecules · 2025Review
- Effect of primary copper metabolism disturbance on elemental, protein, and lipid composition of the organs in Jackson toxic milk mouse.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2025Article
- Hepatolenticular degeneration-induced hepatic dysfunction with extremely atypical clinical manifestations: a Case Report.Frontiers in medicine · 2025Article
- Post-transplant liver biopsies: a concise and practical approach for beginners.Journal of pathology and translational medicine · 2025Review
- Impact of environmental contaminants in fish on cell death and oxidative stress usingFood & nutrition research · 2025Article
- Psychiatric Symptoms in Wilson's Disease-Consequence ofInternational journal of molecular sciences · 2024Review
- Wilson's Disease-Crossroads of Genetics, Inflammation and Immunity/Autoimmunity: Clinical and Molecular Issues.International journal of molecular sciences · 2024Review
- The Role of Glia in Wilson's Disease: Clinical, Neuroimaging, Neuropathological and Molecular Perspectives.International journal of molecular sciences · 2024Review
- A novel tryptanthrin-based "on-off-on" probe for sequential sensing CuAnalytical sciences : the international journal of the Japan Society for Analytical Chemistry · 2024Article
- Copper, Iron, Cadmium, and Arsenic, All Generated in the Universe: Elucidating Their Environmental Impact Risk on Human Health Including Clinical Liver Injury.International journal of molecular sciences · 2024Review
- Modulatory role of welding fumes on serum zinc and copper levels and oxidative stress markers among welders: Considering smoking as a possible implication.Toxicology reports · 2024Article
- Wilson Disease: Copper-Mediated Cuproptosis, Iron-Related Ferroptosis, and Clinical Highlights, with Comprehensive and Critical Analysis Update.International journal of molecular sciences · 2024Review
- Osteochondral lesions in Wilson's disease: case report and literature review.AME case reports · 2024Article
- Challenges and dilemmas in pediatric hepatic Wilson's disease.World journal of hepatology · 2023Review
- Identification of Lncrna-Mrna Networks in Hepg2 Cells uponIranian journal of public health · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Wilson's disease (WD), also known as hepatolenticular degeneration, is an autosomal recessive inherited disorder resulting from abnormal copper metabolism. Reduced copper excretion causes an excessive deposition of the copper in many organs such as the liver, central nervous system (CNS), cornea, kidney, joints, and cardiac muscle where the physiological functions of the affected organs are impaired. The underlying molecular mechanisms for WD have been extensively studied. It is now believed that a defect in P-type adenosine triphosphatase (ATP7B), the gene encoding the copper transporting P-type ATPase, is responsible for hepatic copper accumulation. Deposited copper in the liver produces toxic effects via modulating several molecular pathways. WD can be a lethal disease if left untreated. A better understanding of the molecular mechanisms causing the aberrant copper deposition and organ damage is the key to developing effective management approaches.
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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.