ArticleGut2008
Pathophysiology and fate of hepatocytes in a mouse model of mitochondrial hepatopathies.
Article in Gut, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 51 citations in OpenAlex.
- A novel palmitoylation-based molecular signature reveals COX6A1 as a key regulator in metabolic dysfunction-associated steatotic liver disease.Journal of translational medicine · 2025Article
- Triacylglycerol mobilization underpins mitochondrial stress recovery.Nature cell biology · 2025Article
- Is Autophagy Targeting a Valid Adjuvant Strategy in Conjunction with Tyrosine Kinase Inhibitors?Cancers · 2024Review
- Translatomics reveals the role of dietary calcium addition in regulating muscle fat deposition in pigs.Scientific reports · 2024Article
- Mitochondrial dysfunction reactivates α-fetoprotein expression that drives copper-dependent immunosuppression in mitochondrial disease models.The Journal of clinical investigation · 2023Article
- TRPM8 contributes to liver regeneration via mitochondrial energy metabolism mediated by PGC1α.Cell death & disease · 2022Article
- Differential requirements for mitochondrial electron transport chain components in the adult murine liver.eLife · 2022Article
- Enhanced glycolysis and GSK3 inactivation promote brain metabolic adaptations following neuronal mitochondrial stress.Human molecular genetics · 2022Article
- Scinderin promotes fusion of electron transport chain dysfunctional muscle stem cells with myofibers.Nature aging · 2022Article
- Article
- Mitochondrial respiration controls neoangiogenesis during wound healing and tumour growth.Nature communications · 2020Article
- Mitochondrial disease disrupts hepatic allostasis and lowers the threshold for immune-mediated liver toxicity.Molecular metabolism · 2020Article
- Lipidomics unveils lipid dyshomeostasis and low circulating plasmalogens as biomarkers in a monogenic mitochondrial disorder.JCI insight · 2019Article
- CLPP deficiency protects against metabolic syndrome but hinders adaptive thermogenesis.EMBO reports · 2018Article
- Loss of hepatic LRPPRC alters mitochondrial bioenergetics, regulation of permeability transition and trans-membrane ROS diffusion.Human molecular genetics · 2017Article
- Respiration-Deficient Astrocytes Survive As Glycolytic CellsThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- CLUH regulates mitochondrial metabolism by controlling translation and decay of target mRNAs.The Journal of cell biology · 2017Article
- Schwann cell mitochondria as key regulators in the development and maintenance of peripheral nerve axons.Cellular and molecular life sciences : CMLS · 2017Review
- Hepatocellular autophagy modulates the unfolded protein response and fasting-induced steatosis in mice.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- Mitochondrial cytochrome c oxidase deficiency.Clinical science (London, England : 1979) · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundAlthough oxidative phosphorylation defects can affect the liver, these conditions are poorly understood, partially because of the lack of animal models.
aimsTo create and characterise the pathophysiology of mitochondrial hepatopathies in a mouse model.
methodsA mouse model of mitochondrial hepatopathies was created by the conditional liver knockout (KO) of the COX10 gene, which is required for cytochrome c oxidase (COX) function. The onset and progression of biochemical, molecular and clinical phenotypes were analysed in several groups of animals, mostly at postnatal days 23, 56, 78 and 155.
resultsBiochemical and histochemical analysis of liver samples from 23-56-day-old KO mice showed liver dysfunction, a severe COX deficiency, marked mitochondrial proliferation and lipid accumulation. Despite these defects, the COX-deficient hepatocytes were not immediately eliminated, and apoptosis followed by liver regeneration could be observed only at age 78 days. Hepatocytes from 56-78-day-old KO mice survived despite very low COX activity but showed a progressive depletion of glycogen stores. In most animals, hepatocytes that escaped COX10 ablation were able to proliferate and completely regenerate the liver between days 78 and 155.
conclusionsThe results showed that when faced with a severe oxidative phosphorylation defect, hepatocytes in vivo can rely on glycolysis/glycogenolysis for their bioenergetic needs for relatively long periods. Ultimately, defective hepatocytes undergo apoptosis and are replaced by COX-positive cells first observed in the perivascular regions.
Indexed as
Identifiers
What OpenQuestion holds
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.