ArticleJournal of bioenergetics and biomembranes1999
Stimulation of mitochondrial gene expression and proliferation of mitochondria following impairment of cellular energy transfer by inhibition of the phosphocreatine circuit in rat hearts.
Article in Journal of bioenergetics and biomembranes, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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.
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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.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- The effect of the creatine analogue beta-guanidinopropionic acid on energy metabolism: a systematic review.PloS one · 2013Pooled it
- Low hypoxia tolerance as a determinant of the proinflammatory phenotype: a trained immunity perspective.Frontiers in immunology · 2026Review
- Age-Dependent Decline in Cardiac Function in Guanidinoacetate-Frontiers in physiology · 2019Article
- Intracellular Energy-Transfer Networks and High-Resolution Respirometry: A Convenient Approach for Studying Their Function.International journal of molecular sciences · 2018Review
- Impaired cardiac contractile function in arginine:glycine amidinotransferase knockout mice devoid of creatine is rescued by homoarginine but not creatine.Cardiovascular research · 2018Article
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- Oxidative stress during mitochondrial biogenesis compromises mtDNA integrity in growing hearts and induces a global DNA repair response.Nucleic acids research · 2012Article
- Nuclear-mitochondrial cross-talk in global myocardial ischemia. A time-course analysis.Molecular and cellular biochemistry · 2012Article
- Impaired barrier function by dietary fructo-oligosaccharides (FOS) in rats is accompanied by increased colonic mitochondrial gene expression.BMC genomics · 2008Article
- Relative carnitine deficiency in autism.Journal of autism and developmental disorders · 2004Article
- Heart mitochondria signaling pathways: appraisal of an emerging field.Journal of molecular medicine (Berlin, Germany) · 2004Review
- Effects of hydrogen peroxide on mitochondrial gene expression of intestinal epithelial cells.World journal of gastroenterology · 2002Article
- ATP synthesis is coupled to rat liver mitochondrial RNA synthesis.Molecular and cellular biochemistry · 2001Article
- Proliferation of mitochondria in chronically stimulated rabbit skeletal muscle--transcription of mitochondrial genes and copy number of mitochondrial DNA.Journal of bioenergetics and biomembranes · 2000Article
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 4 institutions in 3 countries.
Funding
Abstract
Mitochondria proliferate when cellular energy demand increases. However, the pathways leading to enhanced expression of mitochondrial genes are largely unknown. We tested the hypothesis that an altered flux through energy metabolism is the key regulatory event by decreasing mitochondrial energy supply to rat heart cells by creatine depletion. Electron microscopy showed that the density of mitochondria increased by 75% in such hearts (p < 0.01). Levels of representative mRNAs encoded on mitochondrial DNA (mtDNA) or on nuclear chromosomes were elevated 1.5 to 2-fold (p < 0.05), while the mtDNA content was unchanged. The mRNA for the nuclear encoded mitochondrial transcription factor A (mtTFA) was increased after GPA feeding (p < 0.05). Thus, we have shown that an impairment of mitochondrial energy supply causes stimulation of gene expression resulting in mitochondrial proliferation, probably as a compensatory mechanism. The observed activation of the mtTFA gene corroborates the important function of this protein in nuclear-mitochondrial communication.
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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.