ArticlePloS one2010
Flavin adenine dinucleotide rescues the phenotype of frataxin deficiency.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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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
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- Unraveling Riboflavin-Mediated Mitochondrial Modulation as a Therapeutic Pathway in Neurological Disorders: An Integrative Systematic Review.The Journal of nutrition · 2026Pooled it
- Triple therapy with darbepoetin alfa, idebenone, and riboflavin in Friedreich's ataxia: an open-label trial.Cerebellum (London, England) · 2013Trial
- Riboflavin in neurological diseases: therapeutic advances, metabolic insights, and emerging genetic strategies.Frontiers in neurology · 2025Review
- Article
- Purification and characterization of recombinant FAD synthetase fromBiochemistry and biophysics reports · 2021Article
- Riboflavin in Neurological Diseases: A Narrative Review.Clinical drug investigation · 2021Review
- Production of riboflavin and related cofactors by biotechnological processes.Microbial cell factories · 2020Review
- Metabolic Alterations inFrontiers in molecular biosciences · 2020Review
- Cell Biology of the Mitochondrion.Genetics · 2017Review
- Metabolic and bioprocess engineering of the yeast Candida famata for FAD production.Journal of industrial microbiology & biotechnology · 2014Article
- Mitochondrial dysfunction induced by frataxin deficiency is associated with cellular senescence and abnormal calcium metabolism.Frontiers in cellular neuroscience · 2014Article
- Article
- Genetic control of biosynthesis and transport of riboflavin and flavin nucleotides and construction of robust biotechnological producers.Microbiology and molecular biology reviews : MMBR · 2011Review
- Current and emerging treatment options in the management of Friedreich ataxia.Neuropsychiatric disease and treatment · 2010Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundFriedreich ataxia is a neurodegenerative disease caused by the lack of frataxin, a mitochondrial protein. We previously demonstrated that frataxin interacts with complex II subunits of the electronic transport chain (ETC) and putative electronic transfer flavoproteins, suggesting that frataxin could participate in the oxidative phosphorylation. METHODS AND
findingsHere we have investigated the effect of riboflavin and its cofactors flavin adenine dinucleotide (FAD) and flavin mononucleotide (FMN) in Saccharomyces cerevisiae and Caenorhabditis elegans models of frataxin deficiency. We used a S. cerevisiae strain deleted for the yfh1 gene obtained by homologous recombination and we assessed growth in fermentable and non-fermentable cultures supplemented with either riboflavin or its derivates. Experiments with C. elegans were performed in transient knock-down worms (frh-1[RNAi]) generated by microinjection of dsRNA frh-1 into the gonads of young worms. We observed that FAD rescues the phenotype of both defective organisms. We show that cell growth and enzymatic activities of the ETC complexes and ATP production of yfh1Delta cells were improved by FAD supplementation. Moreover, FAD also improved lifespan and other physiological parameters in the C. elegans knock-down model for frataxin. CONCLUSIONS/SIGNIFICANCE: We propose that rescue of frataxin deficiency by FAD supplementation could be explained by an improvement in mitochondrial respiration. We suggest that riboflavin may be useful in the treatment of Friedreich ataxia.
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