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- W2056558623 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." @default.
- W2056558623 created "2016-06-24" @default.
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- W2056558623 creator A5067226414 @default.
- W2056558623 creator A5089102708 @default.
- W2056558623 date "2015-03-20" @default.
- W2056558623 modified "2023-10-14" @default.
- W2056558623 title "Wilson’s Disease: A Comprehensive Review of the Molecular Mechanisms" @default.
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- W2056558623 doi "https://doi.org/10.3390/ijms16036419" @default.
- W2056558623 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4394540" @default.
- W2056558623 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25803104" @default.