Oxidative Stress, Glutathione Metabolism, and Liver Regeneration Pathways Are Activated in Hereditary Tyrosinemia Type 1 Mice upon Short-Term Nitisinone Discontinuation

Oxidative Stress, Glutathione Metabolism, and Liver Regeneration Pathways Are Activated in Hereditary Tyrosinemia Type 1 Mice upon Short-Term Nitisinone Discontinuation

Hereditary tyrosinemia type 1 (HT1) is an inherited condition in which the body is unable to break down the amino acid tyrosine due to mutations in the fumarylacetoacetate hydrolase (FAH) gene, coding for the final enzyme of the tyrosine degradation pathway. As a consequence, HT1 patients accumulate...

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Bibliographic Details
Main Authors: Haaike Colemonts-Vroninks, Jessie Neuckermans, Lionel Marcelis, Paul Claes, Steven Branson, Georges Casimir, Philippe Goyens, Geert A. Martens, Tamara Vanhaecke, Joery De Kock
Format: Article
Language:English
Published: MDPI AG 2020-12-01
Series:Genes
Subjects:
hereditary liver disease
tyrosinemia type 1
nitisinone
transcriptomics
oxidative stress
glutathione metabolism
Online Access:https://www.mdpi.com/2073-4425/12/1/3

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https://www.mdpi.com/2073-4425/12/1/3

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