ReviewJournal of bioenergetics and biomembranes1997
Mitochondrial biogenesis in the liver during development and oncogenesis.
Review in Journal of bioenergetics and biomembranes, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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.
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
29 citing papers in PubMed, 102 citations in OpenAlex.
- Tissue-Specific Mitochondrial Functionality and Mitochondrial-Related Gene Profiles in Response to Maternal Nutrition and One-Carbon Metabolite Supplementation During Early Pregnancy in Heifers.Animals : an open access journal from MDPI · 2025Article
- Mitochondrial Dysfunction: Pathophysiology and Mitochondria-Targeted Drug Delivery Approaches.Pharmaceutics · 2022Review
- Article
- Gene expression profiles during postnatal development of the liver and pancreas in giant pandas.Aging · 2020Article
- Giant Island Mice Exhibit Widespread Gene Expression Changes in Key Metabolic Organs.Genome biology and evolution · 2020Article
- Hepatic Gene Expression During the Perinatal Transition in the Rat.Gene expression · 2018Article
- Maternal exercise upregulates mitochondrial gene expression and increases enzyme activity of fetal mouse hearts.Physiological reports · 2017Article
- Regulation of fetal liver growth in a model of diet restriction in the pregnant rat.American journal of physiology. Regulatory, integrative and comparative physiology · 2016Article
- Cellular Glycolysis and The Differential Survival of Lung Fibroblast and Lung Carcinoma Cell Lines.Biomedical sciences instrumentation · 2016Article
- Impact of maternal undernutrition around the time of conception on factors regulating hepatic lipid metabolism and microRNAs in singleton and twin fetuses.American journal of physiology. Endocrinology and metabolism · 2016Article
- MGARP regulates mouse neocortical development via mitochondrial positioning.Molecular neurobiology · 2014Article
- Mitochondrial structure alteration in human prostate cancer cells upon initial interaction with a chemopreventive agent phenethyl isothiocyanate.Cancer cell international · 2014Article
- Activating oxidative phosphorylation by a pyruvate dehydrogenase kinase inhibitor overcomes sorafenib resistance of hepatocellular carcinoma.British journal of cancer · 2013Article
- Aberrant cell proliferation by enhanced mitochondrial biogenesis via mtTFA in arsenical skin cancers.The American journal of pathology · 2011Article
- Mitochondrial bioenergetic adaptations of breast cancer cells to aglycemia and hypoxia.Journal of bioenergetics and biomembranes · 2010Article
- Enrichment of hepatocyte-like cells with upregulated metabolic and differentiated function derived from embryonic stem cells using S-NitrosoAcetylPenicillamine.Tissue engineering. Part C, Methods · 2009Article
- From delocalized lipophilic cations to hypoxia: blocking tumor cell mitochondrial function leads to therapeutic gain with glycolytic inhibitors.Molecular nutrition & food research · 2009Review
- A method for measuring mitochondrial mass and activity.Cytotechnology · 2008Article
- Cardiac PPARalpha Protein Expression is Constant as Alternate Nuclear Receptors and PGC-1 Coordinately Increase During the Postnatal Metabolic Transition.PPAR research · 2008Article
- A message emerging from development: the repression of mitochondrial beta-F1-ATPase expression in cancer.Journal of bioenergetics and biomembranes · 2007Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The analysis of the expression of oxidative phosphorylation genes in the liver during development reveals the existence of two biological programs involved in the biogenesis of mitochondria. Differentiation is a short-term program of biogenesis that is controlled at post-transcriptional levels of gene expression and is responsible for the rapid changes in the bioenergetic phenotype of mitochondria. In contrast, proliferation is a long-term program controlled both at the transcriptional and post-transcriptional levels of gene expression and is responsible for the increase in mitochondrial mass in the hepatocyte. Recently, a specific subcellular structure involved in the localization and control of the translation of the mRNA encoding the beta-catalytic subunit of the H(+)-ATP synthase (beta-mRNA) has been identified. It is suggested that this structure plays a prominent role in the control of mitochondrial biogenesis at post-transcriptional levels. The fetal liver has many phenotypic manifestations in common with highly glycolytic tumor cells. In addition, both have a low mitochondrial content despite a paradoxical increase in the cellular representation of oxidative phosphorylation transcripts. Based on the paradigm provided by the fetal liver we hypothesize that the aberrant mitochondrial phenotype of fast-growing hepatomas represents a reversion to a fetal program of expression of oxidative phosphorylation genes by the activation, or increased expression, of an inhibitor of beta-mRNA translation.
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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.