ReviewIUBMB life2019
Mitochondrial dysfunctions in barth syndrome.
Review in IUBMB life, 2019. 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, 33 citations in OpenAlex.
- Mitochondrial Dysfunctions in Human Primary Coenzyme QBiomolecules · 2026Review
- Clinical and genetic spectrum of pediatric mitochondrial disorders in China: insights from a 47-case genetically confirmed cohort.Orphanet journal of rare diseases · 2026Article
- Tafazzin-deficient zebrafish display mitochondrial dysfunction, neutropenia, and metabolic defects without myopathy.Scientific reports · 2025Article
- Mitochondria-Homing Drug Mitochonic Acid 5 Improves Barth Syndrome Myopathy in a Human-Induced Pluripotent Stem Cell Model and Barth Syndrome Drosophila Model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Allogenic mitochondria transfer improves cardiac function in iPS-cell-differentiated cardiomyocytes of a patient with Barth syndrome.Experimental & molecular medicine · 2025Article
- Mitochondrial diseases: from molecular mechanisms to therapeutic advances.Signal transduction and targeted therapy · 2025Review
- Emerging roles of pyruvate dehydrogenase phosphatase 1: a key player in metabolic health.Frontiers in physiology · 2025Review
- The metabolic basis of inherited neutropenias.British journal of haematology · 2024Review
- Mitochondrial phospholipid metabolism in health and disease.Journal of cell science · 2023Article
- Case report: Variability in clinical features as a potential pitfall for the diagnosis of Barth syndrome.Frontiers in pediatrics · 2023Article
- The Biochemical Assessment of Mitochondrial Respiratory Chain Disorders.International journal of molecular sciences · 2022Review
- The multi-factor modulated biogenesis of the mitochondrial multi-span protein Om14.The Journal of cell biology · 2022Article
- MCU-complex-mediated mitochondrial calcium signaling is impaired in Barth syndrome.Human molecular genetics · 2022Article
- The Influence of Supplemental Dietary Linoleic Acid on Skeletal Muscle Contractile Function in a Rodent Model of Barth Syndrome.Frontiers in physiology · 2021Article
- Studying Lipid-Related Pathophysiology Using the Yeast Model.Frontiers in physiology · 2021Review
- Targeting ER stress and calpain activation to reverse age-dependent mitochondrial damage in the heart.Mechanisms of ageing and development · 2020Review
- Nobiletin: Targeting the Circadian Network to Promote Bioenergetics and Healthy Aging.Biochemistry. Biokhimiia · 2020Review
- Cardiolipin Synthesis in Skeletal Muscle Is Rhythmic and Modifiable by Age and Diet.Oxidative medicine and cellular longevity · 2020Article
- New C-Terminal Conserved Regions of Tafazzin, a Catalyst of Cardiolipin Remodeling.Oxidative medicine and cellular longevity · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Barth syndrome (BTHS) is a rare multisystemic genetic disorder caused by mutations in the TAZ gene. TAZ encodes a mitochondrial enzyme that remodels the acyl chain composition of newly synthesized cardiolipin, a phospholipid unique to mitochondrial membranes. The clinical abnormalities observed in BTHS patients are caused by perturbations in various mitochondrial functions that rely on remodeled cardiolipin. However, the contribution of different cardiolipin-dependent mitochondrial functions to the pathology of BTHS is not fully understood. In this review, we will discuss recent findings from different genetic models of BTHS, including the yeast model of cardiolipin deficiency that has uncovered the specific in vivo roles of cardiolipin in mitochondrial respiratory chain biogenesis, bioenergetics, intermediary metabolism, mitochondrial dynamics, and quality control. We will also describe findings from higher eukaryotic models of BTHS that highlight a link between cardiolipin-dependent mitochondrial function and its impact on tissue and organ function. © 2019 IUBMB Life, 9999(9999):1-11, 2019.
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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.