ArticlePNAS nexus2022
Frataxin controls ketone body metabolism through regulation of OXCT1.
Article in PNAS nexus, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 28 citations in OpenAlex.
- Neuropathology of Friedreich ataxia and its links to metabolic pathways.Neurodegenerative disease management · 2026Review
- Partial bypass of frataxin deficiency by ISCU M141I restores cytosolic and nuclear Fe-S cluster assembly.Cell death and differentiation · 2026Article
- The significance of the ketolytic gene OXCT1 in metabolism, intracellular signaling and disease development.Cellular and molecular life sciences : CMLS · 2026Review
- Integrated methylome-transcriptome profiling reveals epigenetic regulation of immune activation pathways and CSN3-associated lactation repression in bovine subclinical mastitis.Journal of animal science and biotechnology · 2026Article
- The Function and Mechanism of OXCT1 in Tumor Progression as a Critical Ketone Body Metabolic Enzyme.Biomolecules · 2025Review
- Ketone Catabolism Is Essential for Maintaining Normal Heart Function During Aging.Journal of the American Heart Association · 2025Article
- OXCT1 promotes triple negative breast cancer immune escape via modulating succinylation modification of PGK1.Communications biology · 2025Article
- Not Just an Alternative Energy Source: Diverse Biological Functions of Ketone Bodies and Relevance of HMGCS2 to Health and Disease.Biomolecules · 2025Review
- Functional Characterization of Parallel Fiber-Purkinje Cell Synapses in Two Friedreich's Ataxia Mouse Models.Cerebellum (London, England) · 2025Article
- Friedreich ataxia: what can we learn from non-GAA repeat mutations?Neurodegenerative disease management · 2025Review
- Insulin Sensitivity and Insulin Secretion in Adults With Friedreich's Ataxia: The Role of Skeletal Muscle.The Journal of clinical endocrinology and metabolism · 2025Observational
- Skeletal Muscle Involvement in Friedreich Ataxia.International journal of molecular sciences · 2024Review
- Frataxin Loss Promotes Angiotensin II-Induced Endothelial-to-Mesenchymal Transition.Journal of the American Heart Association · 2024Article
- Frataxin deficiency shifts metabolism to promote reactive microglia via glucose catabolism.Life science alliance · 2024Article
- Phenotypic variation of FXN compound heterozygotes in a Friedreich ataxia cohort.Annals of clinical and translational neurology · 2024Article
- A peptide derived from TID1S rescues frataxin deficiency and mitochondrial defects in FRDA cellular models.Frontiers in pharmacology · 2024Article
- Ketolysis is required for the proper development and function of the somatosensory nervous system.Experimental neurology · 2023Article
- Ketolysis is Required for the Proper Development and Function of the Somatosensory Nervous System.bioRxiv : the preprint server for biology · 2023Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Friedreich's ataxia (FRDA) is an autosomal recessive neurodegenerative disease caused by the deficiency of mitochondrial protein frataxin, which plays a crucial role in iron-sulphur cluster formation and ATP production. The cellular function of frataxin is not entirely known. Here, we demonstrate that frataxin controls ketone body metabolism through regulation of 3-Oxoacid CoA-Transferase 1 (OXCT1), a rate limiting enzyme catalyzing the conversion of ketone bodies to acetoacetyl-CoA that is then fed into the Krebs cycle. Biochemical studies show a physical interaction between frataxin and OXCT1 both
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.