ArticleThe application of clinical genetics2019
Barth syndrome: mechanisms and management.
Article in The application of clinical genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed.
- Omega-3 fatty acid supplementation improves skeletal muscle mitochondrial function in a model of Barth syndrome.JCI insight · 2026Article
- Left Ventricular Hypertrabeculation: Historical Evolution, Diagnostic Pitfalls, and a Pragmatic Clinical Approach.Reviews in cardiovascular medicine · 2026Review
- Expanded-access use of elamipretide in a newborn with Barth syndrome: a case report.European heart journal. Case reports · 2025Article
- Mitochondrial cardiomyopathies: navigating through different clinical and management pictures between adult and paediatric forms.Frontiers in cardiovascular medicine · 2025Review
- Mitochondrial bioenergetics and cardiolipin remodeling abnormalities in mitochondrial trifunctional protein deficiency.JCI insight · 2024Article
- Precision Genetic Therapies: Balancing Risk and Benefit in Patients with Heart Failure.Current cardiology reports · 2024Review
- Perturbations in mitochondrial metabolism associated with defective cardiolipin biosynthesis: AnbioRxiv : the preprint server for biology · 2024Article
- Clinical and biochemical footprints of inherited metabolic disease. XVI. Hematological abnormalities.Molecular genetics and metabolism · 2023Review
- Metabolic switch from fatty acid oxidation to glycolysis in knock-in mouse model of Barth syndrome.EMBO molecular medicine · 2023Article
- Clinical and Genetic Screening for Hypertrophic Cardiomyopathy in Paediatric Relatives: Changing Paradigms in Clinical Practice.Journal of clinical medicine · 2023Review
- Elamipretide for Barth syndrome cardiomyopathy: gradual rebuilding of a failed power grid.Heart failure reviews · 2022Review
- Mitochondrial Membranes and Mitochondrial Genome: Interactions and Clinical Syndromes.Membranes · 2022Review
- Review
- Mitochondrial dysfunction in heart failure. Lessons from a hereditary mitochondrial disease.Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology · 2021Article
- Tafazzin Deficiency Reduces Basal Insulin Secretion and Mitochondrial Function in Pancreatic Islets From Male Mice.Endocrinology · 2021Article
- Splicing mutation inActa myologica : myopathies and cardiomyopathies : official journal of the Mediterranean Society of Myology · 2021Article
- Noncompaction Cardiomyopathy-History and Current Knowledge for Clinical Practice.Journal of clinical medicine · 2021Review
- Barth syndrome: cardiolipin, cellular pathophysiology, management, and novel therapeutic targets.Molecular and cellular biochemistry · 2021Review
- 3-Methylglutaric acid in energy metabolism.Clinica chimica acta; international journal of clinical chemistry · 2020Review
- A critical appraisal of the tafazzin knockdown mouse model of Barth syndrome: what have we learned about pathogenesis and potential treatments?American journal of physiology. Heart and circulatory physiology · 2019Review
Corrections and comments
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Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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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.