ArticleJournal of inherited metabolic disease2016
Mitochondrial dysfunction in liver failure requiring transplantation.
Article in Journal of inherited metabolic disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 38 citations in OpenAlex.
- The pivotal role of mitochondria in the pathogenesis and treatment of liver failure: a comprehensive review.Molecular and cellular biochemistry · 2026Review
- MtDNA 3243 A>G mutation and recurrent cholangitis after Kasai procedure in biliary atresia: a case report.Translational pediatrics · 2025Article
- Timing and Indications for Liver Transplantation for Children with Chronic Liver Disease.Children (Basel, Switzerland) · 2025Review
- Protein biomarkers GDF15 and FGF21 to differentiate mitochondrial hepatopathies from other pediatric liver diseases.Hepatology communications · 2024Article
- Hepatic neddylation deficiency triggers fatal liver injury via inducing NF-κB-inducing kinase in mice.Nature communications · 2022Article
- Case Report: Adenosine kinase deficiency diagnosed 10 years after liver transplantation: Novel phenotypic insights.Frontiers in pediatrics · 2022Article
- Pediatric metabolic liver diseases: Evolving role of liver transplantation.World journal of transplantation · 2021Review
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- Hepatic alterations during the development and progression of cancer cachexia.Applied physiology, nutrition, and metabolism = Physiologie appliquee, nutrition et metabolisme · 2020Article
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- GABA, γ-Aminobutyric Acid, Protects Against Severe Liver Injury.The Journal of surgical research · 2019Article
- A Learning Collaborative Approach Increases Specificity of Diagnosis of Acute Liver Failure in Pediatric Patients.Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association · 2018Observational
- Replicative stress and alterations in cell cycle checkpoint controls following acetaminophen hepatotoxicity restrict liver regeneration.Cell proliferation · 2018Article
- Mitochondrial Mutations in Cholestatic Liver Disease with Biliary Atresia.Scientific reports · 2018Article
- Mesenchymal Stem Cells Shift Mitochondrial Dynamics and Enhance Oxidative Phosphorylation in Recipient Cells.Frontiers in physiology · 2018Article
- Lactate and Lactate: Pyruvate Ratio in the Diagnosis and Outcomes of Pediatric Acute Liver Failure.The Journal of pediatrics · 2017Article
- Incidence of Primary Mitochondrial Disease in Children Younger Than 2 Years Presenting With Acute Liver Failure.Journal of pediatric gastroenterology and nutrition · 2016Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
Liver failure is a heterogeneous condition which may be fatal and the primary cause is frequently unknown. We investigated mitochondrial oxidative phosphorylation in patients undergoing liver transplantation. We studied 45 patients who had liver transplantation due to a variety of clinical presentations. Blue native polyacrylamide gel electrophoresis with immunodetection of respiratory chain complexes I-V, biochemical activity of respiratory chain complexes II and IV and quantification of mitochondrial DNA (mtDNA) copy number were investigated in liver tissue collected from the explanted liver during transplantation. Abnormal mitochondrial function was frequently present in this cohort: ten of 40 patients (25 %) had a defect of one or more respiratory chain enzyme complexes on blue native gels, 20 patients (44 %) had low activity of complex II and/or IV and ten (22 %) had a reduced mtDNA copy number. Combined respiratory chain deficiency and reduced numbers of mitochondria were detected in all three patients with acute liver failure. Low complex IV activity in biliary atresia and complex II defects in cirrhosis were common findings. All six patients diagnosed with liver tumours showed variable alterations in mitochondrial function, probably due to the heterogeneity of the presenting tumour. In conclusion, mitochondrial dysfunction is common in severe liver failure in non-mitochondrial conditions. Therefore, in contrast to the common practice detection of respiratory chain abnormalities in liver should not restrict the inclusion of patients for liver transplantation. Furthermore, improving mitochondrial function may be targeted as part of a complex therapy approach in different forms of liver diseases.
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